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BACKGROUND: Parkinson’s disease is a neurodegenerative disease, and its pathogenesis involves mitochondrial dysfunction. Exercise has a potential ameliorative effect on mitochondrial dysfunction related to Parkinson’s disease, but there is no comprehensive review and in-depth analysis in this field. OBJECTIVE: To comprehensively review and analyze mitochondrial dysfunction related to Parkinson’s disease and the potential ameliorative effect of exercise, thereby providing new ideas and methods for the treatment and prevention of Parkinson’s disease. METHODS: We searched the Web of Science, PubMed, CNKI, WanFang, and VIP databases with the keywords of “mitochondria, mitochondrial function, mitochondrial disease, mitochondrial dysfunction, Parkinson’s disease, Parkinson, exercise, physical activity, exercise training, exercise therapy, mitochondrial impairment, mitochondrial damage, mitochondrial defects” in Chinese and “mitochondria, Parkinson’s disease, Parkinson disease, physical exercise, exercise, physical activity, mitochondrial dysfunction, mitochondrial damage, mitochondrial impairment, athletic training, exercise training, rehabilitation” in English. A total of 89 articles were included for review and analysis. RESLUTS AND CONCLUSION: Parkinson’s disease is closely related to mitochondrial dysfunction, including mitochondrial biogenesis inhibition, reduced autophagy, increased apoptosis, abnormal elevation of Ca2+ concentration, and increased oxidative stress in Parkinson’s disease patients. Exercise has a positive effect on mitochondrial dysfunction related to Parkinson’s disease, by promoting mitochondrial biogenesisand autophagy, regulating mitochondrial morphology, altering the plasticity of the mitochondrial respiratory chain, and reducing oxidative stress, thus helping to improve the development and progression of Parkinson’s disease. However, the detailed mechanism between mitochondrial dysfunction and the ameliorative effect of exercise is still not fully understood, and future clinical studies can be conducted to validate the results of animal models and gain insights into the benefits and mechanisms of exercise in patients with Parkinson’s disease. [ABSTRACT FROM AUTHOR]

BACKGROUND: Vitamin C, as an essential nutrient, has a wide range of biological effects and a variety of biological functions related to the pathogenesis of sarcopenia. Vitamin C supplementation is expected to be a novel prevention and treatment measure for sarcopenia. OBJECTIVE: To review recent research advances in the application of vitamin C in the pathogenesis and treatment of sarcopenia, and to discuss the potential role of vitamin C in the prevention and treatment of sarcopenia and possible mechanistic pathways based on published evidence. METHODS: The first author performed a computer search of PubMed, Web of Science, CNKI and other databases for relevant studies involving vitamin C in sarcopenia. The search keywords were “vitamin C, ascorbic acid, L-ascorbic acid, ascorbate, antioxidants, oxidative stress, sarcopenia, muscular atrophy, muscle weakness, muscle development, skeletal muscle regenerate, muscles, skeletal muscle” in English and Chinese, respectively. The search period was from each database inception to July 2023. After screening, 85 articles were included for further review. RESULTS AND CONCLUSION: Ensuring adequate dietary vitamin C intake or maintaining normal circulating levels of vitamin C will help to reduce age-related muscle loss and decrease the prevalence of sarcopenia. In addition, vitamin C supplementation is also useful for improving skeletal muscle mass, strength and physical function with potential synergistic effects in exercise strategies for sarcopenia. The effects of vitamin C on sarcopenia may be via the following biological mechanisms: vitamin C limits the activation of the ubiquitin-proteasome pathway mainly by inhibiting oxidative stress and inflammatory responses in skeletal muscle, thus positively regulating protein metabolic homeostasis, and may enhance mitochondrial antioxidant defenses through its antioxidant effects to maintain healthy mitochondrial function. In addition, vitamin C affects myoblast proliferation, differentiation and myotube size, mainly by increasing the expression of myogenic regulatory factors and activating protein synthesis signaling pathways, which contribute to the promotion of muscle development as well as the repair and regeneration of damaged muscle tissue. The positive effects of vitamin C in sarcopenia need to be studied in large samples and with optimized designs for important influencing factors, such as the choice of supplementation dose and duration, the design of exercise prescription when vitamin C is combined with an exercise intervention, and the assessment of the redox status of the individual. It is recommended that future studies should be conducted in older patients with sarcopenia (< 50 μmol/L) with suboptimal vitamin C status to investigate the efficacy of a combined intervention of long-term supplementation with 1 000 mg/d vitamin C (for 6 months or longer) with at least two or more types of multi-type combined exercise, with supplementation timed to take place at 1 hour after the end of the exercise, and with monitoring of markers of oxidative damage produced during the exercise such as malondialdehyde or protein hydroxyl levels were monitored. In conclusion, the optimal dose and timing of vitamin C supplementation for older adults with sarcopenia needs to be explored more, while the appropriate design of exercise prescriptions (especially the type and intensity of exercise) needs to be further determined. [ABSTRACT FROM AUTHOR]

BACKGROUND: Studies have shown that hesperetin exerts protective effects on chondrocytes through a variety of mechanisms or signaling pathways, but the protective mechanisms have not been fully elucidated. OBJECTIVE: To investigate the effect of hesperetin on lipopolysaccharide-induced inflammatory degeneration of chondrocytes. METHODS: Knee joint chondrocytes from suckling Sprague-Dawley rats were isolated and cultured in vitro, and identified by Safranine O staining. The cytotoxicity of hesperetin on chondrocytes was determined by the MTT assay to ensure the optimal concentration of hesperetin. Chondrocytes were randomly divided into three groups, including the control group, model group, and experimental group. The cellular model of osteoarthritis was established in the latter two groups by simulating chondrocytes with lipopolysaccharide. Chondrocytes in the experimental group was then intervened with hesperetin for 24 hours. Calcein-AM/EthD-I staining was used to detect cell viability. Immunohistochemical staining was performed to determine the expression of type II collagen in chondrocytes. Intracellular reactive oxygen species level was detected by a reactive oxygen species detection kit. Total glutathione level was detected by ELISA. Real-time fluorescent PCR was employed to detect the expression of interleukin 1β, interleukin 6, tumor necrosis factor α and type II collagen. RESULTS AND CONCLUSION: Safranine O staining results showed that the cells extracted were chondrocytes. Cytotoxicity test results showed 0.5 μmol/L hesperetin had the most significant effect on chondrocyte vitality. Compared with the control group, the model group showed a decrease in chondrocyte proliferation ability, an increase in reactive oxygen species levels, a decrease in total glutathione levels, an increase in type II collagen degradation, an increase in the levels of interleukin 1β, interleukin 6, and tumor necrosis factor α, and a decrease in the expression of type II collagen (P < 0.05). Compared with the model group, in the experimental group, the proliferation ability of chondrocytes increased, reactive oxygen species levels decreased, total glutathione levels increased, and type II collagen degradation decreased, levels of interleukin 1β, interleukin 6, and tumor necrosis factor α downregulated, and the expression of type II collagen upregulated (P < 0.05). To conclude, hesperetin has a protective effect on lipopolysaccharide-induced inflammatory degeneration of osteoarthritic chondrocytes, and the mechanism may be associated with inhibition of reactive oxygen species-mediated oxidative stress. [ABSTRACT FROM AUTHOR]

BACKGROUND: Studies have shown that there is a close association between spinal cord injury and ferroptosis, and that tetramethylpyrazine has the function of regulating redox reactions. OBJECTIVE: To investigate the regulatory effect of tetramethylpyrazine on ferroptosis in rats with spinal cord injury and its mechanism. METHODS: Thirty-six female specific pathogen-free Sprague-Dawley rats were randomly divided into sham-operated group, model group and tetramethylpyrazine group, with 12 rats in each group. Animal models of spinal cord injury were established using the modified Allen’s method in the latter two groups. No treatment was given in the sham-operated group, while rats in the model and tetramethylpyrazine groups were given intraperitoneal injection of normal saline and tetramethylpyrazine solution, once a day, for 28 days. RESULTS AND CONCLUSION: The Basso, Beattie & Bresnahan Locomotor Rating Scale score in the tetramethylpyrazine group was lower than that in the shamoperated group but higher than that in the model group after 14, 21, and 28 days of treatment (P < 0.05). After 28 days of treatment, hematoxylin-eosin staining showed that in the model group, the spinal cord tissue of rats showed cavity formation, necrotic tissue and inflammatory infiltration with fibrous tissue formation; in the tetramethylpyrazine group, the area of spinal cord tissue defects was smaller, and inflammatory infiltration and fibrous tissue formation were less than those in the model group. After 28 days of treatment, Prussian blue staining showed that a large amount of iron deposition was seen in the spinal cord tissue of rats in the model group, and less iron deposition was seen in the spinal cord tissue of rats in the tetramethylpyrazine group than in the model group. After 28 days of treatment, the levels of glutathione and superoxide dismutase in the rat spinal cord tissue were decreased (P < 0.05) and the level of malondialdehyde was increased in the model group compared with the sham-operated group (P < 0.05); the levels of glutathione and superoxide dismutase in the rat spinal cord tissue were increased (P < 0.05) and the level of malondialdehyde was decreased in the tetramethylpyrazine group compared with the model group (P < 0.05). After 28 days of treatment, qRT-PCR and western blot assay showed that the mRNA and protein levels of glutathione peroxidase 4, ferritin heavy chain, and ferroportin in the rat spinal cord tissue in the model group were decreased compared with those in the sham-operated group (P < 0.05), while the mRNA and protein levels of glutathione peroxidase 4, ferritin heavy chain, and ferroportin in the rat spinal cord tissue in the tetramethylpyrazine group were increased compared with those in the model group (P < 0.05). Immunofluorescence staining showed that after 28 days of treatment, the neuronal nuclei positive staining in the spinal cord of rats was the most in the sham-operated group and the least in the model group. To conclude, tetramethylpyrazine can improve motor function and play a neuroprotective role in rats with spinal cord injury by regulating ferroptosis. [ABSTRACT FROM AUTHOR]

BACKGROUND: Mesenchymal stem cells are used in flap ischemia-reperfusion injury due to their antioxidant and inflammatory inhibition, and angiogenesis induction. OBJECTIVE: To review the mechanism and latest treatment progress of mesenchymal stem cells in the treatment of flap ischemia-reperfusion injury, and to provide a basis for further theoretical research and clinical rational application. METHODS: We searched the relevant articles indexed in CNKI, WanFang and PubMed databases. Chinese and English search terms were “mesenchymal stem cells; flap ischemia reperfusion injury; conditioned medium; exosomes; oxidative stress; inflammatory reactions; angiogenesis”. Relevant literature since 2010 was searched, and 74 articles were finally included after excluding the literature that had little to do with the topic of the article, poor quality and outdated content. RESULTS AND CONCLUSION: (1) Mesenchymal stem cells play significant roles in antioxidation, inhibition of inflammation and induction of angiogenesis and have great potential in the treatment of flap ischemia-reperfusion injury. (2) However, the defects of mesenchymal stem cells themselves and the decline of therapeutic effect in recent years have put the development and application of mesenchymal stem cells into a bottleneck period, and the research on the plasticity of mesenchymal stem cells conditioned medium and its exosomes and mesenchymal stem cells came into being, and the therapeutic effect was significantly better than the use of mesenchymal stem cells alone. (3) Therefore, a more comprehensive understanding of the mechanism of action and the latest treatment progress of mesenchymal stem cells in the treatment of flap ischemia-reperfusion injury is of great significance for the research of mesenchymal stem cells and the treatment of flap ischemia-reperfusion injury. [ABSTRACT FROM AUTHOR]

BACKGROUND: Current studies have confirmed that Ganoderma lucidum polysaccharides can promote nerve regeneration in neurodegeneration-related diseases. The occurrence of neurodegenerative diseases is closely related to mitochondrial dysfunction, but the role of Ganoderma lucidum polysaccharides on the regulation of apoptosis and mitochondrial function in neurodegenerative diseases is not yet clarified. OBJECTIVE: To explore the regulatory effects and mechanisms of Ganoderma lucidum polysaccharides on apoptosis and mitochondrial dysfunction in H2O2- induced SH-SY5Y cells. METHODS: SH-SY5Y cells were divided into three groups: control group, H2O2 group, and Ganoderma lucidum polysaccharides group. Cells in the control group were normally cultured. Cells in the H2O2 group were treated with 300 μmol/L H2O2 for 24 hours. In the Ganoderma lucidum polysaccharides group, the intervention with 300 μg/L Ganoderma lucidum polysaccharides was conducted first for 1-2 hours, followed by the addition of 300 μmol/L H2O2 for 24 hours. The mitochondrial membrane potential was detected by JC-1 kit. Apoptosis was detected by TUNEL staining kit. The activities of malondialdehyde and superoxide dismutase were detected by malondialdehyde test kit and superoxide dismutase test kit, respectively. The apoptosis and expression of mitochondrial dynamics-related proteins were detected by immunofluorescence staining and western blot assay. RESULTS AND CONCLUSION: (1) Compared with the control group, the mitochondrial membrane potential and superoxide dismutase activity were significantly reduced, as well as apoptotic rate and malondialdehyde levels were significantly increased in the H2O2 group (P < 0.05). After treatment with Ganoderma lucidum polysaccharides, the membrane potential and superoxide dismutase activities were significantly increased, and apoptotic rate and malondialdehyde levels were significantly reduced compared with the H2O2 group (P < 0.05). (2) The expression levels of pro-apoptotic proteins Bax and Caspase-3 were significantly increased, but the expression of anti-apoptotic protein Bcl-2 was significantly decreased in the H2O2 group compared with the control group (P < 0.05). Compared with the H2O2 group, the levels of Bax and Caspase-3 were significantly decreased, but the expression of anti-apoptotic protein Bcl-2 was significantly increased in the Ganoderma lucidum polysaccharides group (P < 0.05). (3) Compared with the control group, the expression of mitochondrial splitting proteins Fis1 and p-Drp1 was significantly increased, but the expression of mitochondrial fusion proteins OPA1, Mfn1, and Mfn2 was decreased in the H2O2 group (P < 0.05). Compared with the H2O2 group, Fis1 and p-Drp1 expression was significantly reduced, but the expression levels of OPA1, Mfn1, and Mfn2 were significantly increased in the Ganoderma lucidum polysaccharides group (P < 0.05). (4) The above results confirm that Ganoderma lucidum polysaccharides can attenuate H2O2-induced oxidative stress damage and apoptosis in SH-SY5Y cells by ameliorating mitochondrial dysfunction. [ABSTRACT FROM AUTHOR]

Copyright of Science & Technology of Food Industry is the property of Science & Technology of Food Industry Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

BACKGROUND: More and more studies have shown that oxidative stress should play an important role in the treatment of osteoporosis. Oxidative stress should cause the accumulation of oxidation activity, which will damage bone-related cells. Finally, it causes the imbalance of bone resorption and bone formation, resulting in a decrease in bone volume and the destruction of the slight structure. Research in recent years has found that some natural products can regulate oxidative stress to treat osteoporosis. The characteristics of extensive sources and small side effects have obvious advantages in the treatment of osteoporosis, and the efficacy is objective. OBJECTIVE: To discuss the mechanism of natural product regulation of oxidation stress in treatment of osteoporosis, conduct a review based on the latest related research progress, provide reference and ideas for more natural products to treat osteoporosis in the future, and provide data support for the clinical application of natural compounds in the treatment of osteoporosis. METHODS: "oxidative stress, free radical, antioxidant, phytotherapy, plant extracts, medicinal plants, herbal medicine, osteoporosis, bone density, bone loss" were used as the keywords in PubMed, Web of Science, Embase, Cochrane, VIP, CBM, WanFang, and CNKI databases to search relevant articles published from January 2010 to February 2023. Inclusion and exclusion criteria were developed, and 64 relevant articles were selected by reading titles, abstracts, and full texts. RESULTS AND CONCLUSION: (1) Some natural products have antioxidant effects and can regulate osteogenic differentiation, osteoblast bone matrix mineralization, osteoclast-mediated bone resorption, proliferation, differentiation, activity, and apoptosis of bone-related cells by improving oxidative stress, thus affecting bone metabolism. (2) These natural products with antioxidant effects play a role in treating osteoporosis by improving bone remodeling balance. (3) The research on the combination of a variety of natural products to improve osteoporosis remains to be explored. (4) The use of natural products to regulate oxidative stress may become a powerful weapon for the clinical treatment of osteoporosis in the future. [ABSTRACT FROM AUTHOR]

Diabetes mellitus erectile dysfunction （DMED） is a common diabetic-related vascular， endocrine and neuropathy in clinical practice， and patients with DMED often present with symptoms such as difficulty in erection， prolonged erection time， poor hardness， and short sexual intercourse. The etiological mechanism is complex， and it is often closely related to many factors such as oxidative stress （OS）， inflammatory response， and neurological and endocrine lesions， which often cross-react and promote the progression of DMED lesions. In recent years， relevant studies have shown that OS and ferroptosis play a key role in DMED: OS can cause neurological and Abnormal endocrine function， decreased synthesis or bioavailability of penile vascular endothelium， spongy endothelial cell dysfunction and decreased smooth muscle diastolic function， resulting in penile erectile dysfunction， and ferroptosis has also been confirmed to be closely related to DMED， controlling OS and ferroptosis to improve erectile function in diabetic patients is a reasonable and effective treatment pathway， but the mechanism of action of ferroptosis leading to DMED needs to be further studied. Therefore， this article reviews the latest information on the correlation between OS and ferroptosis and DMED， aiming to provide a useful reference for exploring the mechanism of DMED， clinical prevention and treatment of DMED， and providing potential directions for future research in this field. [ABSTRACT FROM AUTHOR]

Copyright of Food Research & Development is the property of Food Research & Development Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

BACKGROUND: The development of steroid-induced osteonecrosis of the femoral head is a complex process involving multiple mechanisms. There is still no standard therapeutic drug for early intervention of this disease. Current studies have shown that baicalein has various pharmacological activities such as regulating lipid metabolism, bone metabolism, apoptosis and anti-oxidative stress, which provides an idea for the prevention and treatment of steroid-induced osteonecrosis of the femoral head. OBJECTIVE: To observe the preventive effect of baicalein against steroid-induced osteonecrosis of the femoral head and to investigate its possible mechanism. METHODS: Thirty-six 10-week-old male Sprague-Dawley rats were randomly divided into three groups (n=12 per group): blank control group, model group, and baicalein intervention group. In the model group and baicalein intervention group, intraperitoneal lipopolysaccharide and intramuscular injection of methylprednisolone sodium succinate were performed for modeling, while normal saline was used as a substitute for the modeling drug in the blank control group. Baicalein 300 mg/kg was administered by gavage (once a day for 6 weeks) at the time of initial intramuscular glucocorticoid injection in the baicalein intervention group, and baicalein was replaced by normal saline in the other two groups. The serum level of malondialdehyde in rats was detected at 2 weeks of the experiment. Blood lipid indicators and bone formation metabolic markers were detected at 6 weeks of the experiment, the histomorphometric changes of the femoral head were analyzed by hematoxylin-eosin staining, anti-tartaric acid phosphatase staining and TUNEL staining, and the femoral head was subjected to Micro-CT scanning and three-dimensional reconstruction of the bone in order to analyze the alterations of bone tissue structure and parameters. RESULTS AND CONCLUSION: The serum levels of malondialdehyde, triglyceride, β-collagen type I carboxy-terminal peptide were increased and the serum levels of bone specific alkaline phosphatase and pre-collagen type I amino-terminal peptide were decreased in the model group compared with the blank control group (P < 0.05). The serum level of malondialdehyde decreased in the baicalein intervention group compared with the model group (P < 0.05), but there was no significant difference between the baicalein intervention group and blank control group (P > 0.05). The serum level of triglyceride was higher in the baicalein intervention group than the blank control group (P < 0.05), but had no significant difference between the baicalein intervention group and model group (P > 0.05). There were also no significant differences in the levels of bone specific alkaline phosphatase and β-collagen type I carboxy-terminal peptide between the baicalein intervention group and the other two groups (P > 0.05). The serum level of the baicalein intervention group was lower in the baicalein intervention group than the blank control group (P < 0.05) but had no significant difference between the baicalein intervention group and model group (P > 0.05). Histomorphological analysis of the femoral head showed that the rate of bone empty lacuna, osteoclast counting and cell apoptosis rate in the femoral head of model group rats were significantly higher than those of the other two groups (P < 0.05). There was a significant increase in the number of adipocytes in the bone marrow cavity of the femoral head, bone trabeculae were thinned and sparsely arranged with more disruptions in the continuity. The incidence of osteonecrosis was higher in the model group (75%) than in the baicalein intervention group (25%; bilateral and unilateral exact significance results were both 0.05). There was also an increase in the number of adipocytes in the bone marrow cavity of the femoral head in the baicalein intervention group, and the trabecular changes were roughly similar to those in the model group. Micro-CT results showed that bone volume fraction, trabecular thickness, trabecular number, and bone mineral density decreased and trabecular separation increased in the model group compared with the blank control group (P < 0.05). Overall significant bone mass loss was observed in the model group. Bone tissue parameters in the baicalein intervention group were significantly improved than those in the model group, which were reflected in bone volume fraction, trabecular thickness and trabecular separation (P < 0.05), and trabecular number and bone mineral density had no significant difference between the baicalein intervention group and blank control group (P > 0.05). Although baicalein failed to significantly ameliorate dyslipidemia and promote bone formation in rats with steroid-induced osteonecrosis of the femoral head, it could reduce the incidence of steroid-induced osteonecrosis of the femoral head by reducing oxidative stress damage, decreasing cell apoptosis, inhibiting osteoclasts, suggesting its effectiveness in the early prevention of steroid-induced osteonecrosis of the femoral head. [ABSTRACT FROM AUTHOR]

BACKGROUND: The Yi people have used Sambucus adnata Wall to treat fractures, bruises, arthritis, etc. The author’s group found that the active site aqueous extract (SAW-A) and dichloromethane extract (SAW-B) can promote fracture healing by promoting the expression of genes related to osteoblast proliferation, differentiation and maturation, differentiation and maturation. However, the therapeutic effect of methanol extract (SAW-C) at its active site on osteoarthritis is unclear. OBJECTIVE: To investigate the therapeutic effect of Sambucus adnata Wall extract on osteoarthritis, and to identify the effective targets of Sambucus adnata Wall extract in the treatment of osteoarthritis by network pharmacology technology. METHODS: A rat osteoarthritis model was replicated by anterior cruciate ligamentectomy and model rats were then treated with methanol extract of Sambucus adnata Wall by gavage for 21 days. On the 21st day after modeling, the knee joint of rats was detected by X-ray, the width of the knee joint was measured, oxidative stress indexes and inflammatory factors levels in serum and joint lavage fluid were detected, the morphology of the knee joint was observed by hematoxylin-eosin staining, full-thickness cartilage and hyaline cartilage thickness were measured, and the content of articular cartilage proteoglycan was observed by safranin O-fast green staining. The "drug-component-disease-target" network was constructed. Gene ontology enrichment analysis and Kyoto encyclopedia of genes and genomes enrichment analysis of effective targets were performed, and protein-protein interaction network maps were constructed using cytoscape software. RESULTS AND CONCLUSION: Sambucus adnata Wall extract could reduce tumor necrosis factor-α level in joint lavage fluid and serum levels of prostaglandin E2 and malondialdehyde, while increase the level of superoxide dismutase; relieve joint swelling caused by osteoarthritis; improve the histopathological state of articular cartilage, maintain the thickness of full-thickness articular cartilage, hyaline cartilage and the area of bone trabeculae in subchondral bone; and effectively prevent the loss of proteoglycans in articular cartilage and have a chondroprotective effect. Network pharmacological results showed that the methanol extract of Sambucus adnata Wall may have some targets related to inhibition of tumor necrosis factor, AKT1, interleukin-6, MAPK3, and SRC as well as inhibition of over-activation of EGFR signaling pathway and AGE-RAGE signaling pathway. [ABSTRACT FROM AUTHOR]

Objective To investigate the inhibitory effects of astaxanthin (AST) on pressure overload-induced left ventricular hypertrophy in mice and to explore its molecular mechanism. Methods Twenty-four C57BL/6 wild-type male mice were randomly divided into the following four groups： sham group, sham +AST group, cardiac hypertrophy group, and cardiac hypertrophy +AST group, with 6 in each group. The model of left ventricular myocardial hypertrophy was established by thoracic aorta coarctation (TAC) in the cardiac hypertrophy group and cardiac hypertrophy +AST group. The thoracic aortas of mice in both the sham group and sham +AST group were not ligated. AST ［150 mg/ (kg·d) ］ was intragastrically administered daily from the next day after surgery for 4 weeks in sham +AST group and cardiac hypertrophy +AST group. The mice in sham group and cardiac hypertrophy group were given the same volume of normal saline. After sacrifice, the ratios of heart weight/body weight (HW/BW) and heart weight/tibia length (HW/TL) of mice were measured. The hypertrophy and fibrosis degree of myocardium in mice were observed by HE staining and Picro Sirius Red (PSR) staining, and the cardiomyocyte cross-sectional area and collagen volume fraction were calculated. The mRNA expression levels of atrial natriuretic peptide (ANP), myocardial β isoform (β-MHC), fibrosis-related molecules collagen fiber type Ⅰ (Collα1), and connective tissue growth factor (CTGF) were detected by real-time PCR (RT-PCR). The activity of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) in myocardium were estimated by hydroxylamine method and thiobarbituric acid method, respectively. The protein expression levels of nuclear factor erythroid-derived 2-like 2 (Nrf2) and Heme oxygenase 1 (HO-1) were detected by Western blotting. Results The myocardial structures in the sham group and sham +AST group were neatly arranged without fibrosis. In contrast, the heart volume and fibrosis significantly increased in the cardiac hypertrophy group and cardiac hypertrophy +AST group, and the changes in the cardiac hypertrophy group were more obvious. Compared with the sham group and sham +AST group, the HW/BW, HW/TL, cardiomyocyte cross-sectional area and collagen volume fraction increased in the cardiac hypertrophy group and cardiac hypertrophy +AST group, the mRNA expression levels of ANP,β-MHC, Collα1 and CTGF, and myocardial MDA expression increased, while the protein expression levels of Nrf2 and HO-1, and SOD activity decreased, and the changes in the cardiac hypertrophy group were more significant (all P<0. 05) . Conclusion AST effectively attenuates pressure overload-induced induced left ventricular hypertrophy in mice and its mechanism may be related to reducing the oxidative stress of myocardial tissues by activating Nrf2/HO-1 signaling pathway. [ABSTRACT FROM AUTHOR]

Objective To investigate the effect of retinoid-related orphan receptor a (RORa) overexpression viral vector on doxorubicin-induced cardiotoxicity (DIC) in mice and to explore its potential mechanism. Methods Eighty male C57BL/6 mice were randomly divided into four groups: Con group, DIC group, DIC+RORa group and DIC+ROR+EX527 group, with 20 mice in each group. Mice in the DIC+RORa group and DIC+RORa+EX527 group were injected with adeno-associated virus type 9 (AAV9) vector that overexpressed RORa through the tail vein, while mice in the DIC group were injected with the blank control vector of AAV9. After three weeks of AAV9 vector injection, the DIC mouse model was established by DOX injection through tail vein except for the Con group. DIC+RORa+EX527 group was intraperitoneally injected with SIRT1 specific inhibitor EX527 after each DOX injection. After 4 weeks, left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) were measured using cardiac ultrasonography. Orbital blood and myocardial tissues were taken after death. HE staining was used to observe the pathological changes of myocardial tissues. Serum creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), cardiac troponin I (cTnI), interleukin-1ẞ (IL1ẞ), interleukin-6 (IL-6), and tumor necrosis factor-a (TNF-a) were detected by ELISA. The apoptosis rate was calculated after TUNEL staining, the expression of reactive oxygen species (ROS) in myocardial tissue was detected by DHE staining, the expression levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) in the myocardial tissues were detected by colorimetry method, and the macrophage infiltration and NF-KB p65 expression in the myocardial tissues were observed by immunofluorescence staining. The protein expression levels of cleaved Caspase3. RORa, and SIRT1 were detected by Western blotting, and Ac-NF-кВ р65/NF-кВ р65 and Ac-foxo1/foxol were calculated. The mRNA expression levels of RORa and SIRTI in the myocardial tissues were detected by real-time fluorescent quantitative PCR. Results Compared with the Con group, myocardial fibers in the DIC group were disordered and broken, and the degree of vacuolation of cardiomyocyte was significant. Compared with the DIC group and DIC+RORa+ΕΧ527 group, the degree of myocardial fiber breakage and cardiomyocyte vacuolation were relieved in the DIC+RORa group. LVEF, LVFS, SOD, and GSH-Px were as follows: Con group > DIC+RORa group > DIC group, DIC+RORa+EX527 group (all P<0.05). Serum CK-MB, LDH, cTnI. IL-1B, IL-6, TNF-a, myocardial apoptosis rate, cleaved Caspase-3 protein, ROS, MDA, macrophage infiltration, and NF-KB were as follows: Con group DIC group (all P<0.05). SIRTI mRNA and protein were as follows: Con group, DIC+RORa group> DIC group, DIC+RORa+EX527 group (all P<0.05). Ac-foxol/foxol and Ac-NF-кВ р65/NF-кВ р65 were as follows: Con group. DIC+RORa group < DIC group. DIC+ROR+EX527 group (all P<0.05). Conclusion RORa overexpression viral vector can alleviate DOX-induced myocardial injury, and its mechanism may be related to inhibiting myocardial oxidative stress and inflammatory response through activation of SIRT1 signaling pathway. [ABSTRACT FROM AUTHOR]

In order to provide theoretical support for diabetes prevention and therapy, this study investigated the regulatory effect of Berberis dasystachya Maxim. Polysaccharide (BDP) on glucose and lipid metabolism in streptozotocin (STZ)-induced diabetic rats. Diabetic model rats were randomly assigned to the model control group, low-dose polysaccharide group (BDP-L, 10 mg/kg), mid-dose polysaccharide group (BDP-M, 200 mg/kg), and high-dose group (BDP-H, 400 mg/kg). Blood lipid levels, lipid metabolic enzyme activity, and antioxidant enzyme activity served as evaluation markers. Results showed that after 28 days of administering yellow thorn polysaccharide, the BDP-treated groups exhibited significantly (P<0.05) lower blood glucose and lipid levels compared to the model group, with a remarkable 39.16% reduction in blood glucose in the high-dose group (P<0.01). In contrast, serum insulin levels and hepatic glycogen (HG) levels increased in the BDP-treated groups (P<0.05 or P<0.01), with a 1.28-fold increase in serum insulin (P<0.01) and an 89.79% increase in HG (P<0.01) in the high-dose group. Furthermore, compared to the model group, serum and pancreatic levels of catalase (CAT), superoxide dismutase (SOD), and reduced glutathione (GSH-Px) were significantly elevated (P<0.05 or P<0.01), while malondialdehyde (MDA) levels were considerably reduced (P<0.05) in a dose-dependent manner following BDP treatment. In conclusion, BDP effectively improved glucolipid metabolism in diabetic rats by alleviating oxidative stress, ultimately safeguarding pancreatic β-cell integrity in type I diabetes. [ABSTRACT FROM AUTHOR]

Objective: This study aimed to investigate the effect and mechanism of Liraglutide on high glucose-induced vascular endothelial cell injury. Methods Human umbilical vein endothelial cells (HUVECs) were cultured and divided into 4 groups: control, high glucose stimulation (HG), Liraglutide, and Liraglutide + HG group. ELISA was used to detect the secretion of inflammatory cytokines in each group, kits the levels of intracellular reactive oxygen species (ROS), the activity of SOD2 and Gpx4,and the level of MDA, and Western blot and immun of luorescence method nuclear translocation of Nrf2. Results The HG groupexhibited a significantly higher levels of tumor necrosis factor (TNF-α), interleukin (IL-1), IL-6, as well as the levels of intracellular ROS and MDA, but less activity of SOD2 and Gpx4, less contents of NO, and less nuclear translocation of Nrf2, as compared with the control group. Compared with the HG group, the Liraglutide + HG grouppresented significantly higher levels of TNF-α, IL-1, and IL-6, but lower levels of intracellular ROS and MDA, less activities of SOD2 and Gpx4, less contents of NO and less nuclear translocation of Nrf2. Conclusion Liraglutide suppresses high glucose-induced endothelial cell injury by increasing the nuclear translocation of Nrf2. [ABSTRACT FROM AUTHOR]

BACKGROUND: Oleic acid can regulate inflammation and immune responses, and has the potential to repair skin wounds. Oleic acid has a short retention time at the lesion. It is prone to self oxidation and deterioration in the air, and suitable drug carriers are needed to fully exert the therapeutic effect of oleic acid. OBJECTIVE: To investigate the efficacy of oleic acid-liposome gel in the treatment of chronic burn wounds. METHODS: Oleic acid liposome solution was prepared by thin film dispersion method, and then dissolved in Poloxamer gel matrix to prepare oleic acidliposome gel. (1) In vitro experiment: Oleic acid-liposome gel solution was prepared by adding different volumes of oleic acid-liposome gel into cell medium (volume ratio: 1:3, 1:9, 1:27, respectively). Alma-blue reagent was used to detect the effects of different concentrations of oleic acid-liposome gel on the proliferation of human keratinocytes and human fibroblasts. Crystal violet staining was used to observe cell morphology. (2) In vivo experiment: The animal model of chronic burn wounds was established by using full-thickness burn of SD rat back skin combined with local subcutaneous injection of epirubicin. The 30 successfully modeled rats were randomly divided into five groups with six rats in each group. The wounds of oleic acid liposome gel group, oleic acid group, liposome gel group, positive control group and negative control group were applied with gauze of oleic acid liposome gel, oleic acid, liposome gel, recombinant human epidermal growth factor gel and normal saline. The dressing was changed once every other day. A total of 16 doses were administered. The wound healing was observed. RESULTS AND CONCLUSION: (1) In vitro experiments: Alma-blue reagent detection and crystal violet staining showed that oleic acid liposome gel solution with volume ratio of 1:9 could promote the proliferation of human keratinocytes and human fibroblasts. (2) In vivo experiment: The wound healing time of the oleic acid liposome gel group was shorter than that of the other four groups (P < 0.01), and the wound healing rate at 4, 8, 12, 16, and 20 days was higher than that of the other four groups (P < 0.01). After administration, hematoxylin-eosin staining showed epithelialization and healing of wounds in all five groups, and the epidermal thickness of oleic acid liposome gel group was the closest to normal skin and better than the other four groups. Immunohistochemical staining showed that the expressions of cytokeratin 10, tumor protein 63, α-smooth muscle actin, collagen I, tumor necrosis factor α, interleukin 6, malonaldehyde, and superoxide dismutase in oleic acid liposome gel group were closest to those in normal skin, and superior to those in other four groups. On days 12 and 32 of administration, the expressions of tumor necrosis factor α, interleukin 6, malondialdehyde, and superoxide dismutase in wound homogenate supernatant in oleic acid liposome gel group were closest to those in normal skin, and superior to those in other four groups. (3) The results showed that oleic acid liposome gel could promote the proliferation of keratinocytes and fibroblasts, reduce inflammation and oxidative stress injury, and promote the healing of chronic burn wounds. [ABSTRACT FROM AUTHOR]

Aim To investigate whether SIRT6 overexpression inhibits angiotensin Ⅱ (AngⅡ)-induced cardiomyocyte apoptosis by activating adenosine 5′-monophosphate-activated protein kinase / nuclear factor erythroid 2-related factor 2 / heme oxygenase-1(AMPK/ Nrf2 / HO-1) signaling pathway. Methods The experiment was divided into 4 groups: control group, AngⅡ group,AngⅡ+SIRT6 group, AngⅡ+empty vector (EV) group. The mRNA level of SIRT6 was detected by RT-PCR. The cell activity was measured by MTT assay. The cell apoptosis was analyzed by flow cytometry. SIRT6, cardiomyocyte apoptosis related proteins (Bax, cleaved Caspase-3, Bcl-2), DNA damage related proteins (γ-H2AX, p-ATM), AMPK/ Nrf2 / HO-1 signaling pathway related proteins (p-AMPK, Nrf2, HO-1) were measured by Western blot. The reactive oxygen species (ROS) content was determined by DCFH-DA staining. The changes of the above indexes among the groups were observed. Results Compared with control group, the mRNA and protein expression levels of SIRT6 and cell activity were significantly decreased in AngⅡ group. Apoptosis rate, the expressions of Bax, cleaved Caspase-3 were increased, and the expression of Bcl-2 was decreased. The expressions of γ-H2AX and pATM were increased, and the expressions of p-AMPK, Nrf2, HO-1 were decreased. The activity of ROS was increased (P<0. 01). Compared with AngⅡ+EV group, the expression of SIRT6 and cell activity were significantly increased in AngⅡ+SIRT6 group. Apoptosis rate, the expressions of Bax and cleaved Caspase-3 were decreased, and the expression of Bcl-2 was increased. The expressions of γ-H2AX and p-ATM were decreased, the expressions of p-AMPK, Nrf2, HO-1 were increased. The activity of ROS was decreased (P<0. 01). Conclusion SIRT6 overexpression inhibits AngⅡ- induced cardiomyocyte apoptosis through activation of AMPK/ Nrf2 / HO-1 signaling pathway. [ABSTRACT FROM AUTHOR]

Atherosclerosis is a chronic vascular wall disease and the most common pathological change in cardiovascular disease. Its pathogenesis is closely related to inflammation, oxidative stress, and lipid deposition. Bilirubin itself has biological activities such as antioxidant and anti-inflammatory effects, and has a protective effect on the cardiovascular system. This article summarizes the mechanism of bilirubin in the development of atherosclerosis and its research progress. [ABSTRACT FROM AUTHOR]

To investigate the protective effect and mechanism of magnesium isoglycyrrhizinate (MgIG) on cisplatin (CDDP) -induced myocardial injury in rats. Methods Twenty-four Wistar rats were randomly divided into the normal control group, the cisplatin model group (CDDP group), the cisplatin + magnesium isoglycyrrhizinate low-dose group (MgIG-L group) and the cisplatin + magnesium isoglycyrrhizinate high-dose group (MgIG-H group), with 6 rats in each group. Changes of body mass of rats were monitored daily. At the end of drug administration, cardiac function indexes including left ventricular ejection fraction (LVEF), left ventricular short-axis narrowing rate (LVFS), left ventricular endsystolic internal diameter (LVESD) and left ventricular end-diastolic internal diameter (LVEDD) were detected by echocardiography. The morphology of myocardial tissue was observed by HE staining. Enzyme-linked immunosorbent assay (ELISA) was used to detect serum levels of creatine kinase isoenzyme MB (CK-MB) and troponin I (cTnI). Levels of superoxide dismutase (SOD), malondialdehyde (MDA), glutathione synthase (GSH), reactive oxygen species (ROS) and ferrous ion (Fe2+ ) in homogenates of myocardial tissue were measured biochemically. The protein expressions of nuclear factor E2-associated factor 2 (Nrf2), long-chain fatty acyl coenzyme A synthase 4 (ACSL4), glutathione peroxidase 4 (GPX4) and ferritin heavy chain 1 (FTH1) protein were detected by Western blot assay. Results The body mass of rats in the control group showed an increasing trend during feeding, and the body mass of rats in the CDDP group showed a decreasing trend. Compared with the CDDP group, the body mass of rats in the MgIG-L group and the MgIG-H group increased after 5 d, 9 d and 13 d of treatment (P＜0.05). Compared with the control group, the CDDP group showed decreased LVEF and LVFS, increased LVESD and LVEDD, disturbed myocardial fiber alignment, myocardial fiber degeneration and fracture, increased serum CK-MB and cTnI levels, increased levels of MDA, Fe2+ and ROS in myocardial tissue, decreased levels of SOD and GSH, and decreased levels of Nrf2, GPX4, and decreased FTH1 protein expression levels and increased ACSL4 protein expression levels in myocardial tissue (P＜0.05). Compared with the CDDP group, the above indicators and myocardial histopathological changes were significantly improved in the MgIG-L group and the MgIG-H group. Conclusion Magnesium isoglycyrrhizinate can ameliorate cisplatin-induced myocardial injury by regulating myocardial oxidative stress and inhibiting cardiomyocyte iron death in rats. [ABSTRACT FROM AUTHOR]

The study aims to investigate the anti-aging effect of Silybum marianum extract (SME) on skin aging mice induced by D-galactose (D-gal). The mice were divided into 6 groups. The mouse model of skin aging was induced by subcutaneous injection of D-gal (1 g/ (kg·d)) on the back for 6 weeks. Body weight, skin water content, skin oxidative stress index, HYP and HA levels of mice in each group were measured. HE staining was used to evaluate the skin injury. The relative mRNA expressions of collagen I, collagen III, MMP-1 and MMP-3 in skin were detected by RT-qPCR. The relative expressions of Nrf2 (nucleus), Keap1 and HO-1 in skin were detected by Western blotting. The results show that percutaneous application of all three doses of SME increase the skin water content, alleviate the skin injury, increase the levels of SOD, CAT and GSH-Px, decrease the level of MDA, increased the levels of HYP and HA, increase the relative expression of collagen I and collagen III mRNA, decrease the relative expression of MMP-1 and MMP-3 mRNA, increase the relative expression of Nrf2 (nucleus) and HO-1 protein, and decrease the relative expression of Keap1 protein in D-gal-induced aging mice (P<0.05). ML385 inhibits the activation of Nrf2 pathway and weakens the anti-aging effect of SME (P<0.05). This study shows that percutaneous application of SME has a good anti-aging effect on skin aging mice induced by D-gal, and Nrf2 pathway mediates the anti-aging effect of SME. SME may be a kind of anti-aging daily skin care material with high development value. [ABSTRACT FROM AUTHOR]

The extraction and composition analysis of peptides (FNPs) from fermentation Nannochloropsis sp., as well as their anti-aging effects on Drosophila melanogaster in vivo were investigated. Compared with the non-fermentation group, the number of peptide in FNPs increases by about 100, and the oxidation sites in the peptides also increase. The maximum absorption intensity of FNPs is observed at 258 nm with a dose-dependent relationship. Compared with the control group, 5 μg/mL FNPs extends the mean life span of the the natural aging Drosophila melanogaster for 13 days. Additionally, for 70-90 days old, the deterioration of oxidative stress indicators such as MDA, SOD, and CAT caused by age are significantly restored and increased to the level of positive group by FNPs at 0.5 and 5 μg/mL. These results indicate that FNPs have potential as a promising nutritional component for alleviating human health problems induced by aging. It can also be used as a new antioxidant ingredient for functional food development or cosmeceutical applications from a resource rich and easily obtainable raw material Nannochloropsis sp. [ABSTRACT FROM AUTHOR]

Objective To investigate the effects of Haihuang Bufei Formula on inflammatory factors and T lymphocyte subsets in silicotic rats, and to further explore the therapeutic effects of Haihuang Bufei Formula. Methods The silicotic rat models were constructed by intratracheal instillation of silicon dioxide (SiO2) suspension. After 24 hours of modeling, the rats were randomly divided into normal control group, model group, positive drug control group, and low, medium, high dose group of Haihuang Bufei Formula. Each group contained 10 rats, which were administered once daily for one month. One hour after the last administration, the rats were sacrificed. Lung index, serum tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), hydroxyproline (HYP), superoxide dismutase (SOD), and malondialdehyde (MDA) contents in lung tissue were measured. Hematoxylin-eosin (HE) and Masson staining methods were used to observe the pathological changes in lung tissues. Flow cytometry was used to detect the T lymphocyte subsets in the peripheral blood of rats. Results Compared with the model group, the lung index, serum IL-1β, lung tissue HYP, and MDA contents in the middle and high dose groups of Haihuang Bufei Formula treatment were significantly reduced (P<0.05). In the high-dose group, the serum TNF-α content decreased to (238.64±51.80) ng/L, and the lung tissue SOD content increased to (55.30±13.77) pg/mL (P<0.05). HE and Masson's staining results indicated that the medium and high doses of Haihuang Bufei Formula could alleviate pathological damage of silicosis and fibrosis in lung tissue. Flow cytometer analysis showed that the percentage of CD8+T cells in the high-dose group of Haihuang Bufei Formula was significantly decreased (P<0.05). The ratio of CD4+/CD8+ increased to (1.44±0.19) (P<0.01), and the percentage of CD4+T cells showed no statistically significant change among groups (P>0.05). Conclusions Haihuang Bufei Formula has a protective effect on silicotic rats by reducing collagen content, alleviating pathological damage and fibrosis of lung tissue, which may be related to inhibiting the expression of inflammatory factors, reducing oxidative stress, and regulating the immune system. [ABSTRACT FROM AUTHOR]

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BACKGROUND: Studies have shown that imbalance of bone metabolism during glucocorticoid-induced osteonecrosis of the femoral head necrosis is closely related to oxidative stress. OBJECTIVE: To investigate the pathological mechanism by which oxidative stress-induced ferroptosis promote apoptosis in osteoblasts involved in steroidinduced osteonecrosis of the femoral head. METHODS: General data and serum specimens were collected from 47 patients with steroid-induced osteonecrosis of the femoral head. In addition, six femoral head specimens were collected from these patients. According to the Association Research Circulation Osseous (ARCO) staging system, serum specimens were grouped into ARCO II, III, and IV, while femoral head specimens were classified into ARCO III and IV. Serum levels of malondialdehyde and superoxide dismutase 1 were measured. The protein expression of superoxide dismutase 1, glutathione peroxidase 4, Bcl-2 in the femoral head was detected and verified by Data independent acquisition (DIA) for quantitative sequencing, western blot and alkaline phosphate detection. RESULTS AND CONCLUSION: The ARCO stage of patients with steroid-induced osteonecrosis of the femoral head was independent of age, sex and necrotic side. The serum levels of malondialdehyde and superoxide dismutase 1 were higher in patients with ARCO stage III compared with those with ARCO stage II and IV. The results of DIA protein quantification showed that the function of differential proteins was mainly related to redox. The levels of superoxide dismutase 1, glutathione peroxidase 4, and Bcl-2 in the necrotic region were lower than in the normal region, as well as lower in ARCO stage IV than in ARCO stage III. Western blot verified the results of DIA protein quantification. The alkaline phosphatase activity was lower in the necrotic region than in the normal region, as well as lower in ARCO stage IV than in ARCO stage III. In the necrotic and sclerotic regions, the function of differential proteins was also related to redox, and superoxide dismutase 1, glutathione peroxidase 4, Bcl-2 protein expression and alkaline phosphatase activity were lower in the necrotic area than in the sclerotic region, as well as lower in ARCO stage IV than in ARCO stage III. To conclude, glucocorticoids can influence the progression of steroid-induced osteonecrosis of the femoral head by upregulating oxidative stress levels, inducing osteoblast ferroptosis, and inhibiting osteogenic function. [ABSTRACT FROM AUTHOR]

BACKGROUND: Mitochondrial reactive oxygen bursts have been shown to play a key role in skeletal muscle ischemia-reperfusion injury. 3-Nitro-Nmethylsalicylamide (3-NNMS) can effectively reduce the electron transport rate and has a potential protective effect on limb ischemia-reperfusion injury, but there is no clear research and clinical application. OBJECTIVE: To investigate the protective effect of 3-NNMS on the skeletal muscle after limb ischemia-reperfusion injury in rats and its mechanism. METHODS: Forty healthy 8-week-old Sprague-Dawley rats were randomly divided into control group, 0, 25 and 125 μg/mL 3-NNMS groups, with 10 rats in each group. Animal models of limb ischemia-reperfusion injury were prepared in the latter three groups. 3-NNMS was injected into the injury site 30 minutes before reperfusion. The animals were sacrificed 2 hours after reperfusion. Blood from the apical part of the heart, and the tissue of the rectus femoris muscle of the right lower limb were taken for testing. The pathological morphology of the rectus femoris muscle was detected by hematoxylin-eosin staining. Serum levels of creatine kinase found in the skeletal muscle (CK-MM), lactate dehydrogenase, and myeloperoxidase were detected using ELISA; the levels of nuclear factor κB, tumor necrosis factor α, interleukin 1β, cyclooxygenase 2, malondialdehyde, reactive oxygen species, superoxide dismutase, catalase and glutathione peroxidase in the rectus femoris muscle were measured; and adenosine triphosphate (ATP) level, ATPase activity, and mitochondrial respiratory control rate were tested. RESULTS AND CONCLUSION: Compared with the control group, the model rats with ischemia-reperfusion injury had increased serum levels of CK-MM, lactate dehydrogenase, and myeloperoxidase, increased levels of nuclear factor κB, tumor necrosis factor α, interleukin 1β, cyclooxygenase 2, malondialdehyde and reactive oxygen species in the rectus femoris muscle, decreased levels of catalase and glutathione peroxidase in the rectus femoris muscle, and reduced ATPase activity and mitochondrial respiratory control rate. Moreover, cell morphology was irregular, inflammatory cell infiltration was obvious, and the cells were swollen in rats after ischemia-reperfusion injury. Compared with the 0 μg/mL group, the serum CK-MM and lactate dehydrogenase levels decreased, the levels of nuclear factor κB and cyclooxygenase 2 in the rectus femoris muscle decreased, reactive oxygen species level decreased, and superoxide dismutase activity increased in the 25 μg/mL group; cell morphology was more regular, inflammatory cell infiltration was lighter, and cell swelling was alleviated. Compared with the 0 μg/mL group, the 125 μg/mL group had a reduction in the serum levels of CK-MM, lactate dehydrogenase, and myeloperoxidase and the levels of nuclear factor κB, tumor necrosis factor α, cyclooxygenase 2, malondialdehyde and reactive oxygen species in the rectus femoris muscle, as well as an increase in the levels of superoxide dismutase and glutathione peroxidase in the rectus femoris muscle, and mitochondrial respiratory control rate. Moreover, the cells were arranged neatly, the outline was clear and complete, and the inflammatory cell infiltration was light. To conclude, 3-NNMS can alleviate the functional impairment of the skeletal muscle caused by limb ischemia-reperfusion, and its mechanism of action may be through improving mitochondrial function, reducing reactive oxygen species production, decreasing oxidative stress and inflammatory response, and thus reducing tissue damage and repairing skeletal muscle function. [ABSTRACT FROM AUTHOR]

BACKGROUND: Previous studies have shown that salidroside has an ameliorative effect on multi-organ fibrosis. However, the protective effect of salidroside on angiotensin ii-induced fibrosis in cardiac fibroblasts is unclear OBJECTIVE: To investigate the protective effects of salidroside on angiotensin ii-induced oxidative stress and extracellular matrix deposition in cardiac fibroblasts of Sprague-Dawley rats and its mechanism of action. METHODS: Angiotensin II was used to induce fibrosis in cardiac fibroblasts, and there were five experimental groups: normal control group, model group (final concentration of angiotensin II in culture medium was 1 μmol/L), salidroside low and high dose groups (treatment with salidroside 50, 100 μmol/L for 2 hours, followed by co-incubation with angiotensin II for 48 hours), SIRT1 inhibitor group (treatment with SIRT1 inhibitor EX527 10 μmol/L for 2 hours, followed by high dose of salidroside for 2 hours and then co-incubation with angiotensin II for 48 hours). The cell viability was detected using the cell counting kit-8 method, the cell migration rate was detected by Transwell, the intracellular reactive oxygen species level was detected by DCFH-DA fluorescent probe, and the intracellular malondialdehyde content, superoxide dismutase and catalase activities were detected by relevant kits. The protein and mRNA expression levels of SIRT1, LOXL2, α-SMA, type I collagen and type III collagen were detected by western blot and qRT-PCR, respectively. RESULTS AND CONCLUSION: The cells were identified as cardiac fibroblasts by Vimentin fluorescence. Compared with the normal control group, cell viability, cell migration rate, reactive oxygen species level, and malondialdehyde content were significantly increased, superoxide dismutase and catalase activities were significantly decreased, LOXL2, α-SMA, type I collagen, type III collagen mRNA and protein expression were significantly increased, and SIRT1 protein expression level was significantly decreased in the model group (all P < 0.01). Compared with the model group, the above indexes showed opposite changes in the salidroside low and high dose groups (all P < 0.05). Moreover, salidroside showed dose-dependent regulation. Compared with salidroside groups, cell migration rate and α-SMA protein expression level were significantly increased in the SIRT1 inhibitor group (both P < 0.001). To conclude, salidroside has a protective effect on angiotensin II-induced cardiac fibroblasts and can dose-dependently inhibit oxidative stress and extracellular matrix deposition. [ABSTRACT FROM AUTHOR]

Objective: To investigate the effects of ropivacaine combined with parecoxib sodium serratus plane block (SAPB) on postoperative oxidative stress and immune inflammatory response in patients undergoing thoracoscopic radical resection of lung cancer. Methods: According to the random number table method, 110 patients with lung cancer who underwent thoracoscopic radical resection of lung cancer in The Sixth Affiliated Hospital of Nantong University from January 2021 to April 2023 were divided into observation group (ropivacaine combine with parecoxib sodium SAPB, 55 cases) and control group (ropivacaine SAPB, 55 cases). The postoperative recovery, visual analogue scale (VAS) of pain at rest and cough, immune function, inflammatory response and oxidative stress were compared between two groups, and the incidence of adverse reactions during treatment was observed. Results: The postoperative spontaneous breathing recovery time, eye opening time and extubation time in observation group were shorter than those in control group (P<0.05). The resting VAS and cough VAS in observation group were lower than those in control group 12 h (T2)~48 h (T4) after operation (P<0.05). The levels of superoxide dismutase (SOD), CD3+, CD4+, CD4+/CD8+ in observation group were higher than those in control group at T3 time point. Malondialdehyde (MDA), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and CD8+ were lower than those in control group(P<0.05). The adverse reactions in control group was 7.28%, and that in observation group was 10.92%, with no statistical difference(P>0.05). Conclusion: Ropivacaine combined with parecoxib sodium SAPB for thoracoscopic radical resection of lung cancer, which can effectively improve the clinical symptoms and immune function, reduce the body's inflammatory and oxidative stress. [ABSTRACT FROM AUTHOR]

Objective: To investigate the mechanism by cryptotanshinone regulates the signaling pathway of stromal cell derived factor 1 (SDF-1)/C-X-C chemokine receptor 4 (CXCR4) and inhibits hydrogen peroxide induced cell apoptosis of human bone marrow mesenchymal stem cells (BMSCs). Methods: Cultivated human bone marrow mesenchymal stem cells (HBMSCs) in vitro and established an oxidative stress model by H2O2. Divided HBMSC cells into control group (without oxidative stress induction) and model group (500 μmol/L H2O2 induction for 24 hours), low-dose group of cryptotanshinone(10 μmol/L), medium dose group of cryptotanshinone (20 μmol/L), high-dose group of cryptotanshinone(40 μmol/L). Cell activity was detected by Cell Count Kit (CCK-8). Cell apoptosis was detected by flow cytometry detection. Cellular glucose uptake and lactate levels was detected by enzyme linked immunosorbent assay(Elisa) testing. The content of glutathione (GSH), superoxide dismutase (SOD) and malondialdehyde (MDA) in cells were detected by micro method. Cysteine aspartate protease 3(caspase-3), B-lymphoblastoma-2 associated X protein (Bax), B-lymphoblastoma-2 (Bcl-2), expression of SDF-1 and CXCR4 proteins was detected by western blot detection (Western blot). Results: Compared with the control group, the glucose uptake and lactate levels, GSH, SOD activity, Bcl-2 protein expression, and SDF-1/CXCR4 signaling pathway protein expression of HBMSC cells in the model group decreased, while the cell apoptosis rate, expression of apoptotic protein caspase-3, Bax, and MDA content increased(P<0.05). Compared with the model group, the low, medium, and high dose groups of cryptotanshinone showed an increase in glucose uptake and lactate levels, GSH, SOD activity, Bcl-2 protein expression, and SDF-1/CXCR4 signaling pathway protein expression in HBMSC cells, while the cell apoptosis rate, expression of apoptotic proteins caspase-3, Bax, and MDA content decreased (P<0.05). The differences in various indicators among the low, medium, and high dose groups of cryptotanshinone were statistically significant(P<0.05). Conclusion: Cryptotanshinone may inhibit oxidative stress damage and apoptosis of BMSC induced by hydrogen peroxide by promoting SDF-1/CXCR4 signaling pathway transduction, with high-dose cryptotanshinone having the best effect. [ABSTRACT FROM AUTHOR]

Objective The aim of this study was to investigate the impact and mechanisms of emodin on oxidative stress response in lipopolysaccharide (LPS)-induced murine mononuclear macrophages (RAW264.7). Methods Involved the use of LPS, RAW264.7 cells, and emodin. Experimental groups included a control group, LPS (1 µg/mL) group, and LPS (1 µg/mL) + emodin (15 µmmol/L) pretreatment group. Aldehyde malondialdehyde (MDA) content, intracellular reactive oxygen species (ROS) levels, and silent information regulator 2 (Sirt2) expression were evaluated at 6, 12, and 18 hours after LPS exposure. Additionally, RAW264.7 cells were pretreated with Sirt2 inhibitor AGK2 (20 «mol/L) followed by LPS stimulation, and the above-mentioned parameters were assessed at 6 hours. Results Compared to the control group, MDA content, ROS levels, Sirt2 mRNA, and protein expression in RAW264.7 cells in the LPS group increased at all time points (all P < 0.05). At 6 and 18 hours, MDA content and ROS levels in RAW264.7 cells in the LPS + emodin group decreased significantly (all P < 0.05), while at 12 hours, ROS levels were lower in the LPS group compared to the LPS + emodin group (P < 0.05). Sirt2 mRNA and protein levels significantly increased at all time points (all P < 0.05) compared to the LPS group. In the LPS + emodin + AGK2 group, Sirt2 mRNA and protein levels decreased, and MDA content and ROS levels increased compared to the LPS + emodin group (all P < 0.05) .Conclusion LPS-induced oxidative stress in RAW264.7 cells and emodin attenuate LPS-induced oxidative stress in RAW264.7 cells through Sirt2. [ABSTRACT FROM AUTHOR]

BACKGROUND: The biological behavior of mesenchymal stem cells is influenced by the survival microenvironment. Pre-treatment of the microenvironment is an important means of regulating the function of mesenchymal stem cells. OBJECTIVE: To compare the differences in paracrine function of umbilical cord mesenchymal stem cells and adipose mesenchymal stem cells under oxidative stress and hypoxia, and to provide a theoretical basis for selecting appropriate pretreatment of mesenchymal stem cells to treat different diseases. METHODS: Umbilical cord mesenchymal stem cells and adipose mesenchymal stem cells were cultured by H2O2 or O2 oxygen, respectively, and cell morphology, proliferation, viability and paracrine factor expression were examined. RESULTS AND CONCLUSION: (1) The expression levels of brain-derived neurotrophic factor and transforming growth factor-β were higher in umbilical cord mesenchymal stem cells than in adipose mesenchymal stem cells under a normal culture environment, while the expressions of stromal cell-derived factor-1α and tumor necrosis factor stimulating factor-6 in the adipose mesenchymal stem cells were significantly higher than those in the umbilical cord mesenchymal stem cells. (2) There was no significant difference in the effect of low and moderate levels (≤ 100 μmol/L) of H2O2 on the viability of the two mesenchymal stem cells. However, increasing the H2O2 concentration from 50 μmol/L to 100 μmol/L resulted in a distinct increase in vascular endothelial growth factor expression in umbilical cord mesenchymal stem cells. The expression of basic fibroblast growth factor, vascular endothelial growth factor, stromal cell-derived factor-1α and interleukin-10 in adipose mesenchymal stem cells was greatly increased by increasing H2O2 concentration in this range. (3) 1% O2 hypoxia promoted mesenchymal stem cell proliferation. After 24 hours of culture in 1% O2, gene expression levels were elevated in both mesenchymal stem cells, but the expression levels of vascular endothelial growth factor, interleukin-10 and tumor necrosis factor stimulating factor-6 were significantly higher in adipose mesenchymal stem cells than in umbilical cord mesenchymal stem cells. (4) It is concluded that hypoxia and oxidative stress preconditioning enhances the paracrine function of mesenchymal stem cells. However, mesenchymal stem cells respond differently to hypoxia and oxidative stress. Treating diseases can choose suitable mesenchymal stem cells for appropriate pretreatment to further enhance their therapeutic potential. [ABSTRACT FROM AUTHOR]

Objective: To investigate the protective effect of all-trans retinoic acid （ATRA） on the function of NK cells dam-aged by oxidative stress in liver fibrosis. Methods: Mouse model with liver injury was established by carbon tetrachloride （CCl4）， biochemical and pathological assays were used to evaluate the degree of liver injury and fibrosis in mice， and changes of NK cells and oxidative stress injury in liver tissue of mice were observed. In vitro， NK92 cell lines damaged by H2O2 oxidative stress were evaluated the protective effect of ATRA. Results: Liver inflammation and fibrosis were suppressed and liver function was improved in CCl4 model mice by ATRA treatment. ATRA could increase SOD activity and GSH content in liver tissue， which promoted the proportion and num-ber of hepatic NK cells. ATRA could protect NK cells from oxidative damage and apoptosis induced by H2O2 in vitro. Conclusion: ATRA can ameliorate liver injury and fibrosis induced by CCl4， which may be related to the inhibition of oxidative stress on NK cells. [ABSTRACT FROM AUTHOR]

AIM: To investigate the protective effect of total flavonoids from Patrina villosa Juss (PJF) on the lung in an experimental rat model of acute lung injury (ALI), and to elucidate the potential mechanism. METHODS: The ALI rat model was established by instilling 5 mg/kg of lipopolysaccharide (LPS) into the airway. Sixty male SD rats were randomly divided into 4 groups: control, LPS, LPS+low-dose PJF (receiving 100 mg/kg PJF one hour before ALI modeling) and LPS+high-dose PJF (receiving 300 mg/kg PJF one hour before ALI modeling). Each group consisted of 15 animals. Lung tissues and bronchoalveolar lavage fluid (BALF) were collected from all groups 24 h after modeling. For assessment of lung tissue morphology, HE staining was performed. The wet/dry weight ratio of the lung tissue was determined using the wet/dry weighing method. Evans blue staining was conducted to assess epithelial barrier permeability in lung tissues. ELISA was used to detect the levels of inflammatory factors tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and IL-6 in the BALF, as well as oxidative stress markers including superoxide dismutase (SOD), myeloperoxi-dase (MPO) and glutathione peroxidase (GSH-Px) activity, and malondialdehyde (MDA) content in the lung tissue. The expression levels of C/EBP homologous protein (CHOP), glucose-regulated protein 78 (GRP78) and X-box binding protein 1 (XBP1) in the lung tissue were analyzed by Western blotting. RESULTS: Compared with control group, the rats in LPS group exhibited a blurred alveolar structure with a significant infiltration of inflammatory cells. The ALI score and the wet/dry weight ratio of the lung tissue were increased (P<0. 05). Concurrently, the levels of IL-6, IL-1β and TNF-α in the BALF, along with MDA content and MPO activity in the lung tissue, were elevated (P<0. 05). Additionally, the protein levels of CHOP, GRP78 and XBP1 were up-regulated in the lung tissue (P<0. 05), while the SOD and GSH-Px activity was significantly decreased (P<0. 05). Compared with LPS group, PJF intervention exerted beneficial effects on the lung tissue morphology with reduced ALI score and lower lung wet/dry weight ratio (P<0. 05). Moreover, the levels of IL-6, IL-1β and TNF-α in BALF, as well as MDA content, MPO activity and the protein levels of CHOP, GRP78 and XBP1 in the lung tissue were all significantly decreased (P<0. 05), while the SOD and GSH-Px activity was significantly increased (P<0. 05). The efficacy in high-dose group exceeded that in low-dose group. CONCLUSION: The PJF have protective effect on the lungs of rats with ALI, and its mechanism may be related to the inhibition of inflammation, oxidative stress and endoplasmic reticulum stress. [ABSTRACT FROM AUTHOR]

Objective To investigate the expression and significance of the mechanosensitive ion channel Piezol in human placental chorionic arteries (HPCA) of pre-eclampsia (PE) patients. Methods HPCA tissues were collected from pregnant women undergoing cesarean section delivery at the Department of Obstetrics, Affiliated Hospital of South-west Medical University. The samples included a normal control (NC) group, a PE group, and a severe pre eclampsia (SPE) group, each comprising 10 cases. Immunofluorescence staining was used to detect the expression of Piezol and the endothelial marker CD31 in the HPCA of the NC, PE, and SPE groups. Real-time quantitative PCR (qPCR) was employed to measure the relative mRNA expression of Piezol in the HPCA of the NC, PE, and SPE groups. Western blotting (WB) was conducted to assess the relative protein expression of Piezol in the HPCA of the NC, PE, and SPE groups. Hydrogen peroxide (H2O2) was used to simulate oxidative stress in human umbilical vein endothelial cells (HUVECs), and qPCR and WB were performed to evaluate the mRNA and protein expression of Piezol in the NC group, H2O2, - trea- ted 6 h group, and H2O2 treated 12 h group of HUVECs. Results Piezol co localized with the endothelial marker CD31 in the HPCA tissues of the NC, PE, and SPE groups. The mRNA expression of Piezol showed a decreasing trend in the HPCA tissues of the NC, PE, and SPE groups, with statistically significant differences (P<0.05). Similarly, the protein expression of Piezol exhibited a decreasing trend in the HPCA tissues of the NC, PE, and SPE groups, with statistically significant differences (P<0.05). In HUVECs, both mRNA and protein expression of Piezol showed a decreasing trend in the NC group, H2O2 treated 6 h group, and H2O2 treated 12h group, with statistically significant differences (P<0.05). Conclusion Piezol is expressed in endothelial cells of HPCA tissues, and its abnormal expression may be associated with the pathophysiological changes in pre-eclampsia. The occurrence and development of pre-eclampsia related oxidative stress response may lead to decreased expression of Piezol. [ABSTRACT FROM AUTHOR]

Objective To explore the role and potential mechanisms of all-trans retinoic acid （ATRA） on activation and oxidative stress of hepatic stellate cell （HSC）. Methods Platelet-derived growth factor （PDGF-bb, 10 ng/ml） was applied to induce the activation of HSCs, which was then treated with ATRA at a dosage of 5 μmol/L for 48 h. The effects of ATRA on HSC activation were evaluated by detecting changes in cell growth viability and phenotypic marker expression. The effects of ATRA on HSC oxidative stress were evaluated by detecting changes in intracellular reactive oxygen species （ROS）, reduced glutathione （GSH） and malondialdehyde （MDA）, and the expression of antioxidant genes. The effects of ATRA on HSC autophagic activity were evaluated by detecting changes in autophagy marker expression and autophagic flow. Results Compared with the PDGF-bb group, the cell viability was significantly reduced in ATRA-treated HSCs （ P<0.01）, as well as the expression of α-SMA and Collagen I. The intracellular levels of ROS and MDA were significantly reduced in ATRA-treated HSCs （P<0.01）, whereas the GSH level was significantly increased （P<0.01） . The expression levels of antioxidant genes （NRF2, HO-1, and ATF4）, were significantly higher in ATRA-treated HSCs than those in the normal ones under PDGF-bb condition （P<0.01）. Meanwhile, the expression of autophagy markers Beclin 1 and LC3 Ⅱ/I, and signal of autophagy flow in ATRA-treated HSCs were found to be significantly reduced （P<0.01） . Conclusion ATRA significantly inhibited PDGF-bb-induced HSC activation and reduced the level of oxidative stress and autophagic activity of HSCs, which had potential applications in the prevention and treatment of liver fibrosis. [ABSTRACT FROM AUTHOR]

Objective To explore the effects and mechanisms of deoxycholic acid(DCA)on oxidative stress in human BAR-T cells. Methods The human Barrett epithelial cell line BAR-T was cultured in vitro, and the BAR-T cells were intervened with different concentrations of DCA(100, 200, and 300 μmol/L)and different action time(30 min, 60 min, 3 h and 6 h). The mRNA and protein expression of COX-2 were detected by Real-time PCR and Western blotting assay. The intracellular reactive oxygen species(ROS)content was detected by direct microscope observation and flow cytometry, and was compared with that of 200 μmol/L DCA + 5 mmol/L NAC(ROS scavenger N-acetylcysteine)group; cellular immunofluorescence was used to detect the entry of cellular p65 protein into the nucleus, which was then compared with 200 μmol/L DCA+ PDTC(100 μmol/L, NF-κB pathway inhibitor)group. Results Compared to the control group, DCA increased ROS content in BAR-T cells in a dose-dependent manner. Additionally, 5 mmol/L NAC significantly inhibited DCA-induced ROS release. Furthermore, both 200 μmol/L and 300 μmol/L DCA significantly increased COX-2 mRNA expression compared to the control group at the same intervention time. The 6 h groups for both 200 μmol/L and 300 μmol/L DCA showed a significant increase in COX-2 mRNA expression compared to the 1 h group. Compared to the control group, treatment with 200 μmol/L DCA significantly increased the expression of COX-2 protein. Meanwhile, 200 μmol/L DCA promoted the nucleation of p65 protein, which was inhibited by PDTC. Conclusion DCA activates the NF-κB signaling pathway and upregulates the expression of COX-2 by elevating the intracellular ROS expression and promoting the entry of p65 protein into the nucleus. [ABSTRACT FROM AUTHOR]

Objective: To observe the effects of saphenous nerve pulsed radiofrequency combine with intra-articular injection of sodium hyaluronate on oxidative stress and inflammatory pain mediators in patients with knee osteoarthritis (KOA) who are ineffective in conservative treatment. Methods: 127 KOA patients who were ineffective in conservative treatment in our hospital from July 2021 to December 2022 were selected, according to the random number table method, the patients were divided into control group (n=63, received intra-articular injection of sodium hyaluronate) and combination group (n=64, received saphenous nerve pulsed radiofrequency combine with intra-articular injection of sodium hyaluronate). The knee pain visual analogue (VAS) score, Lysholm knee function score (Lysholm score), inflammatory mediators [interleukin-1β (IL-1β), interleukin-1 (IL-1), tumor necrosis factor-α (TNF-α), pain mediators [substance P (SP), 5-hydroxytryptamine (5-HT), prostaglandin E2 (PGE2 )], oxidative stress indexes [superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), malondialdehyde (MDA)] and adverse reactions were compared between two groups. Results: The VAS score in combination group was lower than that in control group post-treatment, and the Lysholm score was higher than that in control group(P<0.05). MDA in combination group was lower than that in control group post-treatment, GSH-Px and SOD were higher than those in control group (P<0.05). IL-1β, IL-1 and TNF-α in combination group were lower than those in control group post-treatment (P<0.05). SP, 5-HT and PGE2 in combination group were lower than control group post-treatment(P<0.05). There was no difference in the incidence of adverse reactions between two groups(P>0.05). Conclusion: Saphenous nerve pulsed radiofrequency combined with intra-articular injection of sodium hyaluronate can relieve pain, reduce the levels of oxidative stress and inflammatory pain mediators, and promote the recovery of knee joint function in KOA patients with ineffective conservative treatment, and has good safety. [ABSTRACT FROM AUTHOR]

Diabetic retinopathy (DR) is one of the most common microvascular complications of diabetes and has become one of the leading causes of blindness and visual impairment in diabetes patients. The pathogenesis of DR is multifaceted, involving inflammation, oxidative stress, neurovascular abnormalities, and other factors that present potential targets for disease management interventions. Currently, anti-vascular endothelial growth factor (VEGF) drugs serve as the primary treatment for advanced stages of DR when irreversible neurovascular damage and visual impairment have occurred. Additionally, some patients show poor or no response to anti-VEGF treatment. There is a lack of early intervention options for the initial phases of the disease. Therefore, there is an urgent need to develop novel local or systemic therapies based on the underlying mechanisms of DR to enable early prevention and treatment with the aim of preserving patients' vision. Medications targeting various pathways including anti-inflammatory agents (corticosteroids and nonsteroidal anti-inflammatory drugs), neurotrophic and neuroprotective drugs, drugs modulating biochemical pathways, antioxidant phytochemicals, and gene therapy can complement each other in terms of therapeutic effects to benefit a larger number of individuals affected by DR. This article reviews previous research reports on the pathogenesis, drug treatment methods, and potential therapeutic targets associated with DR in order to provide guidance for clinical practice. [ABSTRACT FROM AUTHOR]

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