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BACKGROUND: The low catalytic activity and lack of targeting of commonly used metal ions have severely limited the clinical application of chemodynamic therapy in tumor treatment. On the other hand, although the composite nanoplatforms are endowed with tumor-targeting functions by surface functionalization, the lack of tumor microenvironment acidity also severely weakens the efficacy of chemodynamic therapy. OBJECTIVE: To prepare novel composite nanoplatforms and assess their feasibility to enhance the effects of chemodynamic therapy at the cellular level. METHODS: SLC-0111-loaded zeolite imidazole framework-8 doped with divalent iron ions (Fe2+) and divalent cobalt ions (Co2+) (Fe-Co/ZIF-8@SLC-0111) was synthesized by ion-exchange reaction and self-assembly, and loaded with hyaluronic acid (HA) by electrostatic adsorption, followed by obtaining the target nanoparticles Fe-Co/ZIF-8@SLC-0111-HA (abbreviated as FC-S). Meanwhile, nanoparticles Fe-Co/ZIF-8-HA (abbreviated as FC) without SLC-0111 were synthesized by the same method. The nanocomposite platform was tested for particle size, zeta potential, surface morphology, in vitro reactive oxygen species generation, and ability to consume glutathione. Human osteosarcoma cell MG-63 and mouse fibroblast cell L929 were used as experimental subjects. The cytotoxicity of FC-S was detected by CCK-8 assay. Human osteosarcoma cell MG-63 was used as the experimental object to detect the cell internalization of FC-S. In addition to H2O2, the effects of FC-S and FC on intracellular pH, carbonic anhydrase 9 protein expression, cell viability and apoptosis, intracellular reactive oxygen species and glutathione content, and mitochondrial membrane potential were investigated. RESULTS AND CONCLUSION: (1) The FC-S composite nanoplatform was successfully prepared with a well-defined rhombic dodecahedral structure, uniform size and good dispersion. Its particle size was about 323 nm; zeta potential was about -11.1 mV, and the nanoplatform had a certain reactive oxygen species generation capacity in vitro. (2) FC-S nanoplatforms accumulated intracellularly in a time-dependent manner and could successfully escape from lysosomes. When the mass concentration of FC-S was ≤ 20 µg/mL, there was no obvious cytotoxicity to MG-63 cells and L929 cells, and 20 µg/mL FC-S was selected to act on MG-63 cells in subsequent experiments. (3) Compared with FC group, the protein expression of carbonic anhydrase 9 in MG-63 cells in FC-S group was decreased (P < 0.01); the intracellular acidic environment was enhanced; the content of reactive oxygen species was increased (P < 0.001); the mitochondrial damage was aggravated; the number of dead cells was increased, and the apoptosis rate was increased (P < 0.001). (4) The results indicate that FC-S, as a novel composite nanoplatform, can effectively improve the weakly acidic microenvironment in tumor cells and enhance the level of intracellular reactive oxygen species production, thus enhancing the efficacy of chemodynamic therapy. [ABSTRACT FROM AUTHOR]

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Copyright of Shipin Kexue/ Food Science is the property of Food Science 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.)

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.)

Oxidative stress is the result of imbalance between the formation of reactive oxygen species (ROS) and antioxidant level. Mitochondria are important organelles regulating oxidative stress. Telomerase reverse transcriptase (TERT) not only in the nucleus to maintain telomerase activity and telomere length, but also reversibly transits to mitochondria. Improving the activity of oxidative respiratory chain of mitochondria to reduce the production of mitochondrial reactive oxygen species (mtROS) and to activate GSH system as well as autophagy pathway to promote the clearance of mtROS are all important to down-regulate the level of mtROS, which will alleviate oxidative stress and damage and keep the REDOX balance of cells and the normal function of the body. [ABSTRACT FROM AUTHOR]

Rheumatoid arthritis (RA) is a common chronic autoimmune disease with synovitis as its pathological basis and erosive arthritis as its main symptom. Pathogenesis of RA is complex, combination of genetic factors, environmental factors, immune cells, cytokines and autoantibodies causes joint injury, bone destruction and multi-system disease of RA. However, the above mechanisms can not fully explain the poor prognosis, high disability rate and poor clinical treatment effect of RA. Therefore, exploring new pathogenesis and therapeutic targets of RA is the focus of RA research. In recent years, with the deepening of RA research, it has been found that there is a new form of cell death in pathological process of RA, namely ferroptosis. Ferroptosis is a type of cell death caused by inhibition of glutathione peroxidase activity and accumulation of lipid reactive oxygen species. Previous studies have confirmed the close correlation between RA and ferroptosis, this paper mainly explores ferroptosis-related signal pathways that affect the change and development of RA disease from the perspective of regulating the main signal pathways of ferroptosis, so as to find new therapeutic targets for RA and new therapeutic ideas for research. [ABSTRACT FROM AUTHOR]

Objective: To investigate regulatory effect and mechanism of protein kinase C (PKC)δ/θ-dual functional oxidase 1 (Duox1)-reactive oxygen species (ROS) signaling pathway on human airway mucin (MUC) 5AC, to provide a new target for treatment of high secretion of airway mucus. Methods: Human airway epithelial cells 16HBE were pretreated with PKC and its subunit PKCδ/θ inhibitor, Duox1 inhibitor or free radical scavenger DMTU, respectively, and then human neutrophil elastase (HNE) stimulation to establish an in vitro airway inflammatory cell model. Generation level of ROS in each group of cells was determined by kit, mRNA levels of Duox1 and MUC5AC were detected by real-time fluorescent quantitative PCR, influence of interfering factors of each group of cells on Duox1 protein level was determined by Western blot, and protein expression of MUC5AC in each group of cells was detected by ELISA and immunofluorescence. Results: Compared with control group, ROS production in HNE group was increased significantly, expressions of Duox1 and MUC5AC mRNA and protein were also increased (P<0.05). After administration of Duox1 inhibitors, free radical scavengers or PKC inhibitors and PKCδ/θ inhibitors, ROS production was significantly inhibited, Duox1 and MUC5AC mRNA and protein expressions were decreased (P<0.05), while after giving PKCα/β, ROS generation, Duox1 and MUC5AC mRNA and protein expressions were not significantly changed compared with HNE group (P>0.05). Conclusion: HNE can mediate high expression of MUC5AC through PKCδ/θ-Duox1-ROS, which plays an important role in development of high secretion of airway mucus in vitro cell model experiment. [ABSTRACT FROM AUTHOR]

In this study, the pathogen was obtained from the tea leaves suffering from tea anthracnose by tissue isolation method and identified. Moreover, nano-Cu(OH)2 was prepared by the precipitation method and characterized and the inhibitory activity and inhibition mechanism of nano-Cu(OH)2 on the tea anthracnose pathogen were investigated. The results show that the pathogen isolated from tea leaves clustered with Colletotrichum siamense on the same branch with a self-support rate as high as 91%, confirming the isolated pathogen was C. siamense. The morphology of synthesized nano-Cu(OH)2 were petal-like, bunchy, and clustered nanoparticles, accompanied by an aggregation phenomenon. The highest inhibition rate of 99.16% to C. siamense was achieved at 2 days of treatment 300 mg/L nano- Cu(OH)2 treatment. The Zeta potential of C. siamense was (-8.91± 1.80) mV and that of nano-Cu(OH)2 was (12.55 ± 1.33) mV. The strong antimicrobial effect of nano-Cu(OH)2 might be due to electrostatic interactions. After treatment with nano-Cu(OH)2, the fungal hyphae showed obvious protrusions and distortions, severe damage, and ruptured fungal cell membranes. Concurrently, a significant amount of reactive oxygen species was generated, resulting in the death of most cells. DNA damage measurements showed that nano-Cu(OH)2 treatment caused the tea anthracnose pathogen DNA bands narrower and darker, and as the concentration of nano-Cu(OH)2 increased, the DNA concentration decreased. The results of antioxidant enzyme activity and malondialdehyde (MDA) content measurements showed a decrease in superoxide dismutase (SOD) activity and an increase in MDA content in the fungi. In conclusion, these results suggest that nano-Cu(OH)2 can induce pathogenic cell membrane damage, DNA damage, inhibition of SOD activity, and promotion of MDA production, ultimately leading to cell death. These findings would provide a new approach for the effective control of tea anthracnose using nano-pesticides. [ABSTRACT FROM AUTHOR]

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Copyright of Shipin Kexue/ Food Science is the property of Food Science 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.)

Copyright of Shipin Kexue/ Food Science is the property of Food Science 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.)

Objective To investigate the protective effects of Sulforaphane (SFN) against high glucose (HG)-induced human platelet apoptosis and elucidate the underlying mechanisms in vitro. Methods Purified platelets obtained from healthy individuals were pre-incubated with various concentrations of SFN (5, 10, or 20 μmol/L) or a vehicle control (0.05% DMSO) for 40 minutes at 37 °C. Subsequently, the platelets were stimulated with normal glucose (NG, 5 mmol/L) or high glucose (HG, 25 mmol/L) for an additional duration of 90 minutes. Flow cytometry was employed to assess platelet mitochondrial membrane potential depolarization (Δψm), exposure of phosphatidylserine (PS), and generation of total intraplatelet reactive oxygen species (ROS). Phosphorylation levels of PI3K and Akt were determined using Western blot. Results Compared to NG-treated human platelets, HG significantly induced depolarization of platelet Δψm and exposure of PS (P < 0.001). These effects of HG were markedly attenuated by various concentrations of SFN (P < 0.001). Mechanistically, SFN down-regulated the phosphorylation levels of PI3K (P < 0.01) and Akt (P < 0.05), which were increased by HG when compared to the vehicle control, and substantially reduced total intracellular ROS levels (P < 0.001). The inhibitory effects of SFN on HG-induced phosphorylation of PI3K and Akt, as well as its efficacy on total intracellular ROS generation, Δψm depolarization, and PS exposure in HG-stimulated human platelets were completely reversed by a specific agonist for PI3K, 740 Y-P. Conclusions The current study demonstrates that SFN exerts a protective effect on platelet apoptosis induced by HG, potentially through the down-regulation of the PI3K/Akt-mediated pathway in human platelets in vitro. These findings suggest that SFN may hold promise for improving thrombosis in diabetes mellitus and related chronic metabolic diseases. [ABSTRACT FROM AUTHOR]

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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: Most of the formulas for the clinical treatment of premature ovarian insufficiency have evolved from the basic formula of Liuwei Dihuang Pills, and have achieved good therapeutic efficacy. Currently, most of the experimental studies on Liuwei Dihuang Pills focus on morphological observations and physiological and biochemical detection of in vivo animal models, while fewer studies on molecular mechanisms have been reported. OBJECTIVE: To explore the molecular mechanism of Liuwei Dihuang Pills in the treatment of premature ovarian insufficiency based on the receptor gamma coactivator-1 alpha/mitochondrial transcription factor A/reactive oxygen species pathway. METHODS: Premature ovarian insufficiency model was established in mice by intraperitoneal injection of cyclophosphamide 120 mg/kg combined with busulfan 12 mg/kg, and then Liuwei Dihuang Pill suspension was used to intervene in premature ovarian insufficiency mice. After 12 weeks of intervention, the levels of follicle-stimulating hormone, luteinizing hormone, estradiol, anti-Mullerian hormone, 8-hydroxydeoxyguanosine, total antioxidant capacity and reactive oxygen species in serum of mice were detected by ELISA method. The morphological changes in mouse ovaries were observed by hematoxylin-eosin staining. The ultrastructure of mouse follicular granulosa cells and the apoptosis of granulosa cell mitochondria were observed by transmission electron microscopy. The expression levels of receptor gamma coactivator-1 alpha and mitochondrial transcription factor A in mouse ovarian granulosa cells were detected by immunohistochemistry. RESULTS AND CONCLUSION: Compared with the model group, serum levels of follicle-stimulating hormone, luteinizing hormone, reactive oxygen species, and 8-hydroxydeoxyguanosine were decreased in the experimental group (P < 0.05), and the levels of estradiol, anti-Mullerian hormone, and total antioxidant capacity were increased (P < 0.05). Hematoxylin-eosin staining showed that in the model group, there were more atretic follicles and corpus luteum forms, some secondary follicles, and interstitial fibrosis and hyperplasia; in the experimental group, a large number of atretic follicles, few corpus luteum forms, primordial follicles were observed at the edges but there were few secondary follicles and no mature follicles. Transmission electron microscopy showed that the organelles in ovarian granulosa cells of mice in the experimental groups were relatively intact. Immunohistochemical results showed that compared with the model group, the expression level of receptor gamma coactivator-1 alpha in the ovarian tissue of mice increased slightly in the experimental group at the 4th week, and there was no significant change at the 8th and 12th weeks. The expression level of mitochondrial transcription factor A in the ovarian tissues of mice in the experimental group was transiently increased at the 4th week, and then slightly decreased, which were all significantly different from those of the model group. To conclude, Liuwei Dihuang Pills inhibit ovarian granulosa cell apoptosis in mice with premature ovarian insufficiency to a certain extent through the receptor gamma coactivator-1 alpha/mitochondrial transcription factor A/reactive oxygen species signaling pathway, thereby improving the endocrine function of the ovary, enhancing the antioxidant capacity, and attenuating the degree of oxidative stress damage. [ABSTRACT FROM AUTHOR]

Copyright of Shipin Kexue/ Food Science is the property of Food Science 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.)

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.)

Objective: To discuss the anti-inflammatory and antioxidant effect of mesalazine (MSZ) in the RAW264. 7 cell model, and to elucidate its therapeutic effect on periodontitis in the rats. Methods: The proliferation rates of RAW264. 7 cells stimulated by different concentrations (0, 62. 5, 125. 0, 250. 0, 500. 0, 1 000. 0, and 2 000. 0 mg·L-1 )of MSZ were detected by CCK-8 method to determine the optimal concentration of MSZ for cell treatment. Porphyromonas gingivalis lipopolysaccharide (P. g-LPS) and MSZ were used to treat the RAW264. 7 cells, and the cells were divided into control group, P. g-LPS group, and MSZ+P. g-LPS group. The levels of reactive oxygen species (ROS) in the cells in various groups were detected by the DCFH-DA fluorescent probe assay; the malondialdehyde (MDA) levels, glutathione (GSH) levels and superoxide dismutase (SOD) activities in the cells in various groups were detected by ELISA method; the expression levels of inflammatory factors interleukin-8 (IL-8) and interleukin-1β (IL-1β) mRNA in the cells in various groups were detected by real-time fluorescence quantitative PCR (RT-qPCR) method. The periodontitis rat model was established by the ligation method combined with the injection of P. g bacterial fluid. A total of 18 rats were randomly divided into control group (without treatment), model group (making periodontits model), and drug administration group (making periodontits model and given MSZ), and there were 6 rats in each group. Micro-CT was used to assess the alveolar bone destruction of the rats in various groups; HE staining was used to observe the morphology of periodontal tissue of the rats in various groups. Results: Compared with control group, the proliferation rate of the cells in 500. 0 mg·L-1 MSZ group was significantly increased (P<0. 01), so 500. 0 mg·L-1 MSZ was subsequently selected to treat the cells. Compared with control group, the levels of ROS and MDA in the cells in P. g-LPS group were significantly increased (P<0. 01), and the level of GSH and activity of SOD were significantly decreased (P<0. 01), and the expression levels of IL-1β and IL-8 mRNA were significantly increased (P<0. 01); compared with P. g-LPS group, the levels of ROS and MDA in the cells in MSZ+P. g-LPS group were significantly decreased (P<0. 01), the level of GSH and activity of SOD were significantly increased (P<0. 01), and the expression levels of IL-1β and IL-8 mRNA were significantly decreased (P<0. 01). The micro-CT assay results showed that compared with control group, the distance from the cemento-enamel junction to alveolar bone crest (CEJ-ABC) of the rats in model group was significantly increased (P<0. 01), and the bone volume fraction (BV/TV) was significantly decreaced (P<0. 05); compared with model group; the CEJ-ABC of the rats in drug administration group was decreased (P<0. 01), and the BV/TV was increased (P<0. 05). The HE staining results showed that the inflammatory cell infiltration in periodontal tissue of the rats in drug administration group was reduced, and epithelial attachment was restored. Conclusion: MSZ effectively inhibits the production of pro-inflammatory factors and peroxides in the P. g-LPS-induced RAW264. 7 cells, improves the cellular anti-inflammatory and antioxidant capacity, inhibits the alveolar bone resorption, and alleviates the inflammation of periodontal tissues in the periodontitis rats. [ABSTRACT FROM AUTHOR]

Objective: To discuss the effect of Aspergillus fumigatus (Af) on DNA damage and interleukin (IL)-33 expression in the human bronchial epithelial cells, and to clarify its related mechanism. Methods: Different concentrations (1, 5, and 10 mg·L -1) of Af were used to stimulate the bronchial epithelial BEAS-2B cells to select the appropriate stimulation concentration. When the BEAS-2B cells were treated with N-acetylcysteine (NAC) and Af, the cells were divided into control group, Af group, NAC group, and Af+NAC group. When the BEAS-2B cells were treated with DNA double-strand break repair inhibitor NU7441 and Af, the cells were divided into control group, Af group, NU7441 group, and Af+NU7441 group. The comet assay was used to detect the percentages of comet tail DNA of cells in various groups; immunofluorescence method was used to detect the expression levels of DNA damage-related protein phosphorylated H2AX (γH2AX) in the cells in various groups; 2, 7-dichlorofluorescein diacetate (DCFH-DA) fluorescence probe was used to detect the levels of reactive oxygen species (ROS) in the cells in various groups; real-time fluorescence quantitative PCR (RT-qPCR) method was used to detect the expression levels of interleukih-33 (IL-33), thymic stromal lymphopoietin (TSLP), and interleukih-25 (IL-25) mRNA in the cells in various groups; Western blotting method was used to detect the expression levels of phosphorylated nuclear factor κB (p-NF-κB), phosphorylated ataxia telangiectasia mutated (p-ATM), and γH2AX proteins in the cells in various groups. Results: Compared with control group, the percentage of comet tail DNA and the expression level of γ H2AX in the cells in 1 mg·L-1 Af group showed no significant difference (P>0. 05), while the percentage of comet tail DNA and the expression level of γH2AX in the cells in 5 mg·L -1 Af group were significantly increased (P<0. 01); compared with 5 mg·L-1 Af group, the percentage of comet tail DNA and the expression level of γH2AX in the cells in 10 mg·L-1 Af group were significantly increased (P<0. 01). Compared with control group, the ROS levels in the bronchial epithelial cells in 1 mg·L-1 Af group was significantly increased (P< 0. 05); compared with 1 mg·L-1 Af group, the ROS level in the cells in 5 mg·L-1 Af group was significantly increased (P<0. 01); compared with 5 mg·L-1 Af group, the ROS level in the cells in 10 mg·L-1 Af group was significantly increased (P<0. 05). After treatment of NAC, compared with Af group, the percentage of comet tail DNA (P<0. 01), the expression level of γH2AX (P<0. 05), and the ROS level (P<0. 01) in the cells in Af+NAC group were significantly decreased; after treatment of NU7441, compared with Af group, the percentage of comet tail DNA and the expression level of γH2AX in the cells in Af+NU7441 group were significantly increased (P<0. 01). The RT-qPCR results showed that after treatment of NAC, compared with control group, the expression level of IL-33 mRNA in the cells in Af group was significantly increased (P<0. 05); compared with Af group, the expression level of IL-33 mRNA in the cells in Af+NAC group was significantly decreased (P<0. 05); after treatment of NU7441, compared with Af group, the expression level of IL-33 mRNA in the cells in Af+NU7441 group was significantly increased (P<0. 05). The Western blotting results showed that after treatment of NAC, compared with control group, the expression levels of p-NF-κB, p-ATM, and γH2AX proteins in the cells in Af group were significantly increased (P<0. 05); after treatment of NU7441, compared with Af group, the expression levels of p-NF- κB, p-ATM, and γH2AX proteins in the cells in Af+NAC group were significantly decreased (P<0. 05); After treat ment of NU7441, compared with Af group, the expression levels of p-NF- κB, p-ATM, and γH2AX proteins in the cells in Af+NU7441 group were significantly increased (P<0. 05). Conclusion: Af promotes the IL-33 expression in the human bronchial epithelial cells by causing DNA damage, and its mechanism may be related to the activation of ATM/NF-κB signaling pathway. [ABSTRACT FROM AUTHOR]

Objective: To discuss the alleviative effect of ginsenoside Rg1 on chronic intermittent hypoxia (CIH)-induced brain injury in the mice, and to clarify its possible mechanism. Methods: Forty male C57BL/6 mice were randomly divided into control group, model group, inhibitor group (treated with calpain-1 inhibitor), low dose of ginsenoside Rg1 group (treated with 10 mg·kg-1 ginsenoside Rg1), and high dose of ginsenoside Rg1 group (treated with 20 mg·kg-1 ginsenoside Rg1). Except for the control group, the mice in all other groups were placed in a hypoxic chamber with automatically regulated oxygen concentration to induce hypoxic brain injury. The peripheral blood oxygen saturation (SpO2) of tail of the mice in various groups was detected; the escape latencies and path lengths and the frequency of swimming route crossing the target quadrant of the mice in various groups were determined by Morris water maze test; the levels of blood urea nitrogen (BUN), lactate (LA), malondialdehyde (MDA), interleukin-6 (IL-6), and tumor necrosis factor- α (TNF- α) and the activities of superoxide dismutase (SOD) and lactate dehydrogenase (LDH) in serum of the mice in various groups were detected by kits; the degrees of brain tissue injury of the mice in various groups were observed by HE staining. The levels of reactive oxygen species (ROS) in CA1 region of hippocampus tissue of the mice in various groups were detected by dihydroethidium (DHE) probe; the expression levels of calpain-1, IL-6, and TNF- α proteins in brain tissue of the mice in various groups were detected by Western blotting method. Results: Compared with control group, the SpO2 of the mice in model group was significantly decreased (P<0. 01), indicating that the model was successfully established. Compared with model group, the SpO2 of the mice in inhibitor group, low dose of ginsenoside Rg1 group and high dose of ginsenoside Rg1 group were significantly increased (P<0. 01). The Morris water maze test results showed that compared with control group, the escape latency and path length of the mice in model group were significantly prolonged (P<0. 01), and the frequency of swimming route of crossing the target quadrant was significantly decreased; compared with model group, the escape latencies and path lengths of the mice in inhibitor group, low dose of ginsenoside Rg1 group and high dose of ginsenoside Rg1 group were significantly shortened (P<0. 01), and the frequency of swimming route of crossing the target quadrant was significantly increased. Compared with control group, the levels of BUN, LA, MDA, IL-6, and TNF-α in serum of the mice in model group were significantly increased (P<0. 01), while the activity of LDH was significantly increased (P<0. 01), and the activity of SOD was significantly decreased (P<0. 01); compared with model group, the levels of BUN, LA, MDA, IL-6, and TNF-α in serum of the mice in inhibitor group, low dose of ginsenoside Rg1 group and high dose of ginsenoside Rg1 group were significantly decreased (P<0. 01), while the activities of LDH were significantly decreased (P<0. 01), and the activities of SOD were significantly increased (P<0. 01). The HE staining results showed that compared with control group, the pyramidal neurons in CA1 region of hippocampus tissue of the mice in model group were loosely arranged, while some neurons were triangular, with nuclear pyknosis, cytoplasmic hyperchromasia, and a few neurons were lost, indicating obvious hypoxic neuronal injury; compared with model group, the hypoxic neuronal injury in CA1 region in hippocampus tissue of the mice in inhibitor group, low dose of ginsenoside Rg1 group and high dose of ginsenoside Rg1 group was effectively alleviated. The DHE probe detection showed that compared with control group, the level of ROS in CA1 region in hippocampus tissue of the mice in model group was significantly increased (P<0. 01); compared with model group, the levels of ROS in CA1 region in hippocampus tissue of the mice in inhibitor group, low dose of ginsenoside Rg1 group and high dose of ginsenoside Rg1 group were significantly decreased (P<0. 01). The Western blotting results showed that compared with control group, the expression levels of calpain-1, TNF-α, and IL-6 proteins in hippocampus tissue of the mice in model group were significantly increased (P<0. 01); compared with model group, the expression levels of calpain-1, TNF- α, and IL-6 proteins in hippocampus tissue of the mice in inhibitor group, low dose of GRg1 group and high dose of GRg1 group were significantly decreased (P<0. 01). Conclusion: Ginsenoside Rg1 can alleviate brain tissue injury of the mice induced by CIH; its mechanism may be related to the inhibition of brain tissue inflammatory response and oxidative stress, and the downregulation of calpain-1 expression. [ABSTRACT FROM AUTHOR]

Objective: To discuss the effect of curcumin on ameliorating doxorubicin (DOX) -induced cytotoxicity in the H9c2 cardiomyocytes, and to clarify its mechanism. Methods: The H9c2 cardiomyocytes were treated with DOX to establish the cardiotoxicity model. The H9c2 cells were divided into normal group, DOX group, DOX+curcumin group, and DOX+curcumin+silent information regulator 3 (SIRT3) inhibitor-3 (3-TYP) group. After 24 h, the morphology of the cells in various groups were observed; CCK-8 method was used to detect the viabilities of the cells in various groups; TUNEL staining was used to detect the apoptotic rates of the cells in various groups; enzyme-linked immunosorbent assay (ELISA) method was used to detect the activities of catalase (CAT) and superoxide dismutase (SOD) and the levels of malondialdehyde (MDA) in the cells in various groups; 2, 7-dichlorofluorescein diacetate (DCFH-DA) staining was used to detect the levels of reactive oxygen species (ROS) in the cells in various groups; Western blotting method was used to detect the expression levels of B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX2), NADPH oxidase 4 (NOX4), SIRT3, acetylated superoxide dismutase 2 (Ac-SOD2), and superoxide dismutase 2 (SOD2) proteins in the cells in various groups. Results: Compared with normal group, the H9c2 cells in DOX group exhibited swelling, the activity of the cells was decreased (P< 0. 05), the CAT and SOD activities were decreased (P<0. 05), the MDA and ROS levels were increased (P<0. 05), the expression levels of NOX2, and NOX4 proteins were increased (P< 0. 05), the ratio of Bcl-2/Bax and the expression level of SIRT3 protein were decreased (P<0. 05), and the expression levels of SOD2 and Ac-SOD2 proteins were increased (P<0. 05). Compared with DOX group, the H9c2 cells in DOX+curcumin group showed improved morphology, the activity of the cells was increased (P<0. 05), the CAT and SOD activities were increased (P<0. 05), the MDA and ROS levels were decreased (P<0. 05), the expression levels of NOX2, and NOX4 proteins were decreased (P< 0. 05), the ratio of Bcl-2/Bax and the expression level of SIRT3 protein were increased (P<0. 05), and the expression levels of SOD2 and Ac-SOD2 proteins were decreased (P<0. 05). Compared with DOX+ curcumin group, the cells in DOX+curcumin+3-TYP group exhibited swelling, the activity of the cells was decreased (P<0. 05), the apoptotic rate of the cells was significantly increased (P<0. 05), the CAT and SOD activities were decreased (P<0. 05), the MDA and ROS levels were significantly increased (P<0. 05), the expression levels of NOX2 and NOX4 proteins were increased (P<0. 05), the ratio of Bcl-2/Bax and the expression level of SIRT3 protein were decreased (P<0. 05), and the expression levels of SOD2 and Ac-SOD2 proteins were increased (P<0. 05). Conclusion: Curcumin suppresses the oxidative stress and apoptosis by activating the SIRT3/SOD2 signaling pathway, improving the cell activity and alleviating the DOX-induced cytotoxicity in the H9c2 cells. [ABSTRACT FROM AUTHOR]

Aim To investigate the effect of theaflavin on oxidized low density lipoprotein (ox-LDL)-induced foam cell formation and oxidative stress in THP-1 macrophages and its mechanism. Methods THP-1 derived macrophages were pretreated with 50 μmol/L theaflavin and (or) 10 μmol/L nuclear factor erythroid 2-related factor 2 (NRF2) inhibitor ML385, then 100 mg/L ox-LDL was added to the cells for 24 h to establish the foam cell model. The effect of theaflavin on THP-1 macrophages viability was evaluated by CCK-8 assay and LDH release. The expression of inflammatory cytokines interleukin-6 (IL-6), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) were analyzed by real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot. The release of inflammatory cytokines were detected by enzyme linked immunosorbent assay (ELISA). Intracellular lipid accumulation was detected by Oil red O staining, and lipid absorption was observed by DiL-labeled oxidized low density lipoprotein (DiL-ox-LDL) staining. Reactive oxygen species (ROS) level was detected by DCFH-DA probe. The expression of lipid uptake, cholesterol efflux and oxidative stress-related proteins were detected by Western blot and RT-qPCR. Results Treatment with 100 mg/L ox-LDL significantly decreased cell viability and cholesterol efflux-related protein expressions, increased lipid uptake, accumulation and lipid uptake-related protein expressions, and significantly promoted inflammation and ROS level, as well as the expressions of myeloperoxidase (MPO), NADPH oxidase 2 (NOX2) in THP-1 macrophages (all P<0. 05). After pretreatment with theaflavin, cell viability was increased, intracellular lipid uptake, accumulation and lipid uptake-related protein expressions were significantly reduced, cholesterol efflux-related protein expressions were significantly increased, the expression and release of IL-6, IL-1β and TNF-α were significantly decreased, ROS level was significantly decreased, and the expression of MPO and NOX2 were decreased (all P<0. 05). Pretreatment with theaflavin effectively alleviated intracellular oxidative stress by altering the expression of NRF2, heme oxygenase-1 (HO-1) and Kelch-like ECH-associated protein 1 (KEAP1) in NRF2 signaling pathway, and enhanced the translocation of NRF2 into the nucleus. After pretreatment with ML385, the expression levels of NRF2, HO-1, KEAP1 and CD36 were significantly decreased. Conclusion Theaflavin can significantly inhibit ox-LDL-induced foam cell formation, inflammation, and oxidative stress through NRF2/HO-1 signaling pathway in THP-1 macrophages. [ABSTRACT FROM AUTHOR]

Traditional sunscreens, especially organic ultraviolet (UV) absorbers such as benzophenone, have strong photoactivity and skin permeability, which may cause some human injuries and even cancer. Therefore, it is of great practical significance to develop efficient and safe new sunscreen. With anhydrous zinc acetate (Zn(Ac)2), titanium tetrachloride (TiCl4) and dopamine hydrochloride as raw materials and ethanol/water solution as solvent, polydopamine (PDA) coated Zn-Ti layered double hydroxide (P@ZTL) compounded particles were synthesized through a hydrothermal method. Afterwards, sunscreen samples were prepared with them as the only UV-blocking component. The chemical structure, composition and micro- morphology, along withUV absorbance, free radical scavenging and cytotoxicity performance of P@ZTL were studied. Indispensably, the UV-blocking properties of the sunscreen samples were tested. The results showed that the structure of P@ZTL was 1~5 μm PDA coated ZTL compounded particles, with a specific surface area of 145. 916 m2/g. The particles had a typical mesoporous structure with a porosity of 0. 154 cm3/g. The compounded particles had great UV absorption and reactive oxygen species(ROS)scavenging abilities, along with no cytotoxicity. The sunscreen with P@ZTL had excellent UV protecting performance, which could preserve fibroblasts from direct UV irradiation. The sun protection index(SPF)values of sunscreen samples added with 10% and 15% P@ZTL reached 47. 3±2. 3 and 75. 1±3. 1, respectively, which could fully meet the daily use. Therefore, the synthesized P@ZTL sunscreen has a great application prospect in cosmetics. [ABSTRACT FROM AUTHOR]

Ferroptosis and disulfidpthosis are associated with various diseases. Ferroptosis is distinguished by abnormal accumulation of iron ions and lipid reactive oxygen species, while disulfidptosis is marked by abnormal accumulation of disulfides. Solute carrier family 3 member 2 (SLC3A2), a component of the solute carrier family, is implicated not only involved in the regulation of tumor cell proliferation, migration, invasion and apoptosis, but also in the processes of ferroptosis and disulfidptosis, playing a pivotal role in tumor growth and progression. This article provides an overview of the latest advancements in understanding the relationship between SLC3A2 and ferroptosis, disulfidptosis and tumors, aiming to establish a theoretical basis for targeted cancer therapies. [ABSTRACT FROM AUTHOR]

AIM: To explore the promotion of ferroptosis by artesunate (Art) and its underlying mechanism in osteosarcoma. METHODS: Human osteosarcoma U-2 OS cells were divided into 4 groups: control, ferrostatin-1 (Fer-1), Art, and Art+Fer-1 groups. Cell viability was measured by CCK-8 assay, while reactive oxygen species (ROS), Fe2+, and glutathione (GSH) levels were measured using biochemical assays. Mitochondrial morphology was evaluated by transmission electron microscopy. The mRNA and protein levels of p53, solute carrier family 7 member 11 (SLC7A11) and glutathione peroxidase 4 (GPX4) were determined by RT-qPCR and Western blot, respectively. RESULTS: It was found that Art significantly reduced the growth of U-2 osteosarcoma cells, as well as inducing ferroptosis by promoting the accumulation of Fe2+ and ROS and reducing GSH levels, while the ferroptosis inhibitor ferrostatin-1 inhibited ferroptosis. It was also observed that Art affected mitochondrial morphology, resulting in smaller mitochondria, higher mitochondrial membrane density, and reduced numbers of cristae. Treatment with Art also downregulated both the mRNA and protein expression of the ferroptosis-associated genes SLC7A11 and GPX4, while upregulating expression of p53, an upstream regulator of ferroptosis, thus inducing ferroptosis. CONCLUSION: Artesunate induces ferroptosis in osteosarcoma cells through the p53/SLC7A11/GPX4 signaling pathway. [ABSTRACT FROM AUTHOR]

Objective: To investigate the effect of wogonin (WOG) on hypoxia/reoxygenation (H/R)-induced cardiomyocyte apoptosis by regulating adenosine monophosphate-activated protein kinase (AMPK)/NOD-like receptor protein 3 (NLRP3) signaling pathway. Methods: H9C2 cells were divided into Control group (normal culture), H/R group (H/R induction), L (low dose)-WOG group, M (medium dose)-WOG group, H (high dose)-WOG group (40, 80, 120 µmol/L WOG were added on the basis of H/R induction), WOG+Compound C group (10 µmol/L AMPK inhibitor Compound C was added on the basis of H-WOG group). The effect of WOG on the proliferation of H9C2 cells was detected by methyl thiazolyl tetrazolium (MTT) assay and 5-ethynyl-2'-deoxyuridine (EdU) staining. The effect of WOG on apoptosis of H9C2 cells was detected by flow cytometry. The levels of serum oxidative stress indexes [malondialdehyde (MDA), reactive oxygen species (ROS), superoxide dismutase (SOD)] and inflammatory factors [interleukin (IL)-1B, IL-18] in H9C2 cells were detected by enzyme-linked immunosorbent assay (ELISA). The expression of AMPK, NLRP3, B cell lymphoma-2 (Bcl-2) and Bcl-2 associated X protein (Bax) in H9C2 cells was detected by Western blot (WB). Results: The optical density (OD), EdU positive cell rate, SOD, AMPK and Bcl-2 of H9C2 cells in H/R group were lower than those in Control group, and the apoptosis rate, IL-1B, IL-18, ROS, MDA, NLRP3 and Bax were higher than those in Control group (P<0.05). Compared with H/R group, OD490, EdU positive cell rate, SOD, AMPK and Bcl-2 expression in L-WOG group, M-WOG group and H-WOG group increased, while apoptosis rate, IL-1B, IL-18, ROS, MDA, NLRP3 and Bax decreased (P<0.05). The OD, EdU positive cell rate, SOD, AMPK and Bcl-2 in WOG+Compound C group were lower than those in H-WOG group, and the apoptosis rate, IL-1B, IL-18, ROS, MDA, NLRP3 and Bax expression were higher than those in H-WOG group (P<0.05). Conclusion: WOG can inhibit H/R-induced cardiomyocyte apoptosis, which may be relate to the AMPK/NLRP3 signaling pathway. [ABSTRACT FROM AUTHOR]

Objective To evaluate the protective effect and underlying mechanism of ulinastatin on hepatic ischemia-reperfusion injury. Methods Twenty-four male SD rats were divided into three groups: sham operation group (Sham group), hepatic ischemia-reperfusion injury group (HIRI group) and hepatic ischemia-reperfusion injury + ulinastatin pretreatment group (HIRI+UTI group), with 8 rats in each group. The HIRI rat models were established by occluding hepatic portal vein and hepatic artery for 1 h. In the HIRI+UTI group, the rats were intraperitoneally injected with ulinastatin at 30 min before model establishment, and an equivalent amount of normal saline was given in the Sham and HIRI groups. The rats were sacrificed at 6 h after model establishment. Serum samples were collected to detect alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels. Pathological changes of liver tissues were observed by hematoxylin-eosin (HE) staining. Ultrastructural changes of mitochondria in liver tissues were observed by transmission electron microscopy. The expression of glutathione peroxidase 4 (GPX4) was determined by immunofluorescent staining. The contents of malondialdehyde (MDA), glutathione (GSH), Fe, reactive oxygen species (ROS) and GPX4 were detected. The expression levels of GPX4 and acyl-CoA synthetase long-chain family 4 (ACSL4) messenger RNA (mRNA) and proteins in liver tissue were measured. Results Compared with the Sham group, serum ALT and AST levels were up-regulated, pathological changes such as congestion, hepatocyte necrosis and abnormal hepatic lobule structure were observed, pathological score was increased, the mitochondria shrank, the membrane density was increased, the mitochondrial crest was damaged or even absent, the contents of ROS, MDA and Fe were elevated, the GSH content was decreased, the fluorescent intensity of GPX4 was weakened, the relative expression levels of ACSL4 mRNA and protein were up-regulated, and the relative expression levels of GPX4 mRNA and protein were down-regulated in the HIRI group (all P<0.05). Compared with the HIRI group, serum ALT and AST levels were down-regulated, liver tissue injury was alleviated, pathological score was decreased, mitochondrial shrinkage and crest breakage were mitigated, the contents of ROS, MDA and Fe were down-regulated, the GSH content was up-regulated, the fluorescent intensity of GPX4 was enhanced, the relative expression levels of ACSL4 mRNA and protein were down-regulated, and the relative expression levels of GPX4 mRNA and protein were up-regulated in the HIRI+UTI group (all P<0.05). Conclusions Ulinastatin may alleviate hepatic ischemia-reperfusion injury in rats probably through inhibiting ferroptosis. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Contemporary Pediatrics is the property of Xiangya Medical Periodical Press 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.)

As a natural macromolecular protein extracted from silk, silk fibroin (SF) has been widely used as biological material in recent years due to its antioxidant and photodamage reduction effects. To study the protective effect of silk fibroin against skin photodamage, the immortalized human keratinocyte line (HaCaT) was used as a model for study of UVB injury. Intracellular reactive oxygen species (ROS) and the levels of calcium ions (Ca2+) were measured by ELISA and fluorescence microscopy. The expression of transient receptor potential cation channel subfamily V member 1 (TRPV1) and the expression of Claudin-1 were detected by immunofluorescence assay. In addition, western blotting was used to analyze the expression of tight junction proteins occludin and Claudin-1. The results showed that 120 mJ/cm2 of UVB stimulation significantly reduced cell viability, while the presence of 100 μg/mL silk fibroin significantly increased cell viability. UVB stimulation could increase the level of intracellular ROS, activate TRPV1 channels, and induce the increase of intracellular Ca2+ level. Meanwhile, the levels of inflammatory cytokines interleukin- 1α (IL-1α) (P<0.01) and S100A8 (P<0.05) were also significantly increased, which caused inflammation. However, the effect of UVB on HaCaT cells with the addition of silk fibroin was significantly decreased (P<0.05). In conclusion, UVB could disrupt the structural integrity of barrier proteins, resulting in the decreased expression of the barrier proteins Claudin-1 and occludin. The addition of silk fibroin could reduce such effect and protect the tightly connected structure. Therefore, silk fibroin might have great potential to protect skin from UV-induced inflammation, barrier damage and oxidative stress damage. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Chinese Institute of Food Science & Technology / Zhongguo Shipin Xuebao is the property of Journal of Chinese Institute of Food Science & Technology Periodical 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.)

Copyright of Journal of Chinese Institute of Food Science & Technology / Zhongguo Shipin Xuebao is the property of Journal of Chinese Institute of Food Science & Technology Periodical 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.)

Copyright of Shipin Kexue/ Food Science is the property of Food Science 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.)

Copyright of Journal of Guangdong University of Technology is the property of Journal of Guangdong University of Technology 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.)

Copyright of Journal of Clinical Nursing in Practice is the property of Journal of Clinical Nursing in Practice (Editorial Board, Shanghai Jiao Tong University Press) 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.)

Objective To explore whether the environmental pollutant triclosan (TCS) has negative effects on the various biological characteristics of dental pulp stem cells (DPSCs), as well as the distribution and hazards of TCS in rat dental pulp tissue in vivo, which will provide a basis for the clinical application of DPSCs and the safety of TCS. Methods Tooth collection was approved by the Ethics Committee of Tianyou Hospital Affiliated to Wuhan University of Science and Technology. Human DPSCs were extracted, cultured, and identified. Up to 0.08 mmol/L of TCS was added to the in vitro culture medium of DPSCs. The proliferation ability of DPSCs was detected by CCK-8. The migration ability of DPSCs was detected via scratch assay. The differentiation ability of DPSCs was detected by inducing trilineage differentiation. The gene or protein expression levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-10 (IL-10), inducible nitric oxide synthase (iNOS), and transforming growth factor-β (TGF-β) in DPSCs were detected. The level of reactive oxygen species (ROS) generated by DPSCs was analyzed using fluorescence staining. Changes in mitochondrial membrane potential of DPSCs were detected using a fluorescent probe. The activity of PI3K/Akt/mTOR, p38, and JNK pathways of DPSCs were detected. Animal experiments were approved by the Animal Ethics Committee of Wuhan University of Science and Technology. A rat model of short-term oral exposure to 50 mg/kg/d of TCS for 2 months was established, and the TCS concentration in the liver, brain, and dental pulp tissues of rats was detected through liquid chromatography-mass spectrometry. Results TCS at 0.02 mmol/L, 0.04 mmol/L, and 0.08 mmol/L significantly inhibited the proliferation ability of human-derived DPSCs on the 5th and 7th days of contact. TCS at 0.04 mmol/L and 0.08 mmol/L significantly inhibited the migration ability and tri-lineage differentiation ability of DPSCs on the 3rd day of contact. TCS induced the gene or protein expression of proinflammatory factors including TNF-α, IL-1β, IL-6, and iNOS, induced the gene or protein expression of TGF-β, and inhibited the protein expression of anti-inflammatory factor IL-10. On day 1, TCS at 0.04 mmol/L and 0.08 mmol/L induced the production of ROS in DPSCs and reduced the mitochondrial membrane potential of DPSCs. On day 3, TCS at these levels inhibited PI3K/Akt/mTOR pathway activity and enhanced p38 pathway activity of DPSCs, without affecting the pathway activity of JNK. After short-term intragastric exposure of rats to TCS, TCS was detected in liver (430 ng/mL) and brain (41.4 ng/mL) tissues but not in the dental pulp. The TCS concentration was highest in the liver, but no obvious histopathological changes were observed. Conclusion TCS inhibits a variety of biological characteristics of DPSCs and poses a potential risk to the organism. No TCS exists in the dental pulp tissue of rats exposed to TCS for a brief period of time, and the health of the rats is not damaged.

Oxidative stress is the result of imbalance between the formation of reactive oxygen species (ROS) and antioxidant level. Mitochondria are important organelles regulating oxidative stress. Telomerase reverse transcriptase (TERT) not only in the nucleus to maintain telomerase activity and telomere length, but also reversibly transits to mitochondria. Improving the activity of oxidative respiratory chain of mitochondria to reduce the production of mitochondrial reactive oxygen species (mtROS) and to activate GSH system as well as autophagy pathway to promote the clearance of mtROS are all important to down-regulate the level of mtROS, which will alleviate oxidative stress and damage and keep the REDOX balance of cells and the normal function of the body.

Objective: To study the effect of betulinic acid (BA) on dextran sodium sulfate (DSS)-induced ulcerative colitis. Methods: Eighty-four C57BL/6 mice were randomly divided into 7 groups, namely control, BA (0.5 mg/kg), DSS (4% by mass), low-, medium- and high-dose (0.25, 0.5 and 1 mg/kg) BA + DSS, and 5-aminosalicylic acid (5-ASA) (50 mg/kg) + DSS groups. BA or 5-ASA was gavaged continuously for 14 days, and 4% DSS solution was consumed every day from the 8th day to induce colitis in mice for 7 consecutive days. Afterwards, the length of the colon was measured, the pathological changes and ultrastructure were observed by hematoxylin and eosin (H&E) staining and transmission electron microscopy, the level of reactive oxygen species (ROS) was measured by immunofluorescence staining, inflammatory factors were detected by real-time polymerase chain reaction (real-time PCR), and cell apoptosis was observed by TUNEL staining. Results: After DSS treatment, the length of the colon was significantly decreased (P < 0.05), the arrangement of intestinal crypts became disordered with irregular surfaces, and the number of goblet cells was reduced, which was accompanied by incomplete intestinal tight junctions and sparse microvilli. Meanwhile, DSS induced the accumulation of ROS and significantly up-regulated the mRNA levels of the inflammatory cytokines interleukin-1β (IL-1β), IL-6, and IL-10 (P < 0.01), down-regulated the mRNA expression of tumor necrosis factor-α (P < 0.01) in the colon, and promoted cell apoptosis (P < 0.01). However, pretreatment with either BA or 5-ASA could reverse these phenomena, and the effect of BA was better than that of 5-ASA. Conclusion: BA has a preventive or protective effect against DSS-induced colitis by improving the integrity of intestinal structure, reducing ROS production, improving the inflammatory response and inhibiting apoptosis.

BACKGROUND: Rheumatoid arthritis is an inflammatory disease. Many studies have shown that wogonin has a good anti-inflammatory effect on rheumatoid arthritis, but its exact efficacy and specific mechanism of action remain to be clarified. OBJECTIVE: To investigate the mechanism of wogonin ameliorating joint inflammation by regulating endoplasmic reticulum stress pathway in rats with collagen- induced arthritis. METHODS: (1) At the animal level: Female Wistar rats were divided into healthy control group, arthritis model group and wogonin treatment group. Rat models of arthritis in the latter two groups were established by subcutaneous injection of bovine type II collagen and adjuvant. In the wogonin group, wogonin was given by gavage for 28 consecutive days after modeling. During this period, the rats in each group were weighed, and arthritis score and ankle swelling were measured every 7 days. After the experiment, the pathological changes of the joint were observed, the mRNA and protein levels of endoplasmic reticulum stress pathway GRP78 and CHOP were detected by qRT-PCR, western blot, and immunohistochemistry. (2) At the cellular level, cell counting kit-8 was used to detect the cytotoxic effect of wogonin on fibroblast-like synoviocytes from rats with collagen-induced arthritis. The fibroblast-like synoviocytes induced by thapsigargin were treated with different concentrations of wogonin. The levels of interleukin-1β and tumor necrosis factor-α in the cell supernatant were detected by ELISA, and the intracellular reactive oxygen species in each group were determined by DCFH-DA probe method. The mRNA and protein levels of GRP78, IRE1α, XBP1s and CHOP were detected by qRT-PCR and western blot, respectively. RESULTS AND CONCLUSION: Compared with the healthy control group, arthritis index score and ankle swelling degree in the arthritis model group were increased (P < 0.01), synovial hyperplasia, inflammatory cell infiltration, cartilage destruction and bone erosion were observed in pathological sections, and the mRNA and protein expressions of GRP78 and CHOP in the ankle were significantly increased (P < 0.01), which were mainly located in synovial tissue and articular surface. Compared with the arthritis model group, the arthritis index score and ankle swelling degree in the wogonin treatment group were decreased (P < 0.05), synovial hyperplasia and the number of inflammatory cells were decreased, cartilage destruction and bone erosion were alleviated, the mRNA and protein expression levels of GRP78 and CHOP in the ankle were decreased (P < 0.05), particularly in synovial tissue and on the articular surface. There was no significant difference in body mass among the three groups (P > 0.05). In the cell experiment, 200 μmol/L wogonin significantly reduced the survival rate of fibroblast-like synoviocytes (P < 0.01). Compared with the blank control group, the levels of interleukin-1β, tumor necrosis factor-α, content of reactive oxygen species, and mRNA and protein expression of GRP78, IRE1α, XBP1s, and CHOP in the thapsigargin group were significantly increased (P < 0.05); compared with the thapsigargin group, 50 and 100 μmol/L wogonin significantly reduced the levels of interleukin-1β and tumor necrosis factor-α in the cell supernatant (P < 0.05, P < 0.01), and 100 μmol/L wogonin significantly reduced the content of reactive oxygen species (P < 0.01) and down-regulated the mRNA and protein expression levels of GRP78, IRE1α, XBP1s and CHOP (all P < 0.05). These results suggest that wogonin can effectively alleviate joint inflammatory responses in rats with collagen-induced arthritis, and the endoplasmic reticulum stress pathway may be the key target of its intervention. [ABSTRACT FROM AUTHOR]

BACKGROUND: Precision therapy based on multifunctional nanomaterials is a novel therapeutic model for malignancies that can integrate multiple imaging and therapeutic models into one nanoscale platform to achieve visual combination treatment. OBJECTIVE: To prepare novel nanoparticles loaded with Cu2(OH)PO4 nanoparticles (CuNPs) and nuciferine (NF) (h-PCuNF), and to explore their ability to mediate combined photothermal therapy/photodynamic therapy/chemodynamic therapy/chemotherapy for malignancy. METHODS: The h-PCuNF nanoparticles were synthesized through a double-emulsion procedure, through which the CuNPs and NF were loaded into the shell of hollow poly(lactic-co-glycolic) acid nanocarriers. The morphology, structure, particle size, and zeta potential of the h-PCuNF nanoparticles were characterized. In deionized water, the magnetic resonance imaging and photothermal conversion performances of the h-PCuNF nanoparticles, as well as their capability to implement reactive oxygen species production by mediating photocatalysis and Fenton-like reactions, were evaluated. In liver malignant tumor cell line HepG2 cells, the effectiveness of the photothermal therapy/photodynamic therapy/chemodynamic therapy/chemotherapy combination therapy mediated by the nanoparticles was detected by employing fluorescence imaging and MTT assay. RESULTS AND CONCLUSION: (1) The h-PCuNF nanoparticles possessed a hollow spherical structure in which the CuNPs (drug loading rate and encapsulation rate were 26.3% and 63.2%, respectively) and NF (drug loading rate and encapsulation rate were 11.0% and 52.6%, respectively) were loaded into the shell. The average particle size of the h-PCuNF nanoparticles was (309.2±10.0) nm, while the zeta potential was determined to be (-12.5±0.9) mV. In physiological environments, the nanoparticles possess favorable suspension stability. (2) In deionized water, the h-PCuNF nanoparticles could markedly enhance T1-weighted magnetic resonance imaging images. The h-PCuNF nanoparticles showed remarkable photothermal conversion and photocatalytic reactive oxygen species generation capabilities under near infrared laser irradiation. In addition, the h-PCuNF nanoparticles could consume glutathione and mediate Fenton-like reactions to produce OH. (3) The h-PCuNF nanoparticles could be taken up by HepG2 tumor cells and were mainly distributed in the cytoplasm. The synergistic therapeutic effect was demonstrated after the nanoparticles were activated by near infrared laser irradiation, because CuNPs mediated photothermal therapy/ photodynamic therapy/chemodynamic therapy and NF mediated chemotherapy could synergistically eliminate the tumor cells. [ABSTRACT FROM AUTHOR]

BACKGROUND: During healing process of chronic wounds, excessive production of reactive oxygen species can impair the function of L929 fibroblasts, thereby delaying wound repair. Therefore, protecting fibroblasts from oxidative stress is important to promote wound healing. OBJECTIVE: To assess the protective effects of carboxymethyl chitosan-oxidized chondroitin sulfate/platelet-rich plasma (CMC-OCS/PRP) hydrogel on L929 cells under H2O2 stimulation. METHODS: CMC-OCS/PRP hydrogels were prepared, and the micromorphology, degradation performance, scavenging ability of H2O2 and hydroxyl radical and biocompatibility of the hydrogels were characterized. L929 cells with good growth state were taken and cultured in five groups. The control group was cultured conventionally. H2O2 was added to the H2O2 group. Carboxymethyl chitosan-oxidized chondroitin sulfate hydrogel extract + H2O2 was added to the CMC- OCS group. Platelet-rich plasma gel extract + H2O2 was added to the PRP group. The CMC-OCS/PRP group was treated with carboxymethyl chitosan-oxidized chondroitin sulfate/platelet-rich plasma hydrogel extract + H2O2. Each group was treated with hydrogel extract for 6 hours, and then H2O2 for 24 hours. After culture, the levels of active oxygen and malondialdehyde, apoptosis and expression of collagen fiber I protein were detected. In the presence of H2O2, the above hydrogel extracts were directly or indirectly co-cultured with L929 fibroblasts for 36 hours, respectively. Migration ability of the cells was detected by scratch test and Transwell chamber test. RESULTS AND CONCLUSION: (1) CMC-OCS/PRP hydrogels had uniform and interrelated porous structure and good degradation ability, could effectively remove H2O2 and hydroxyl radicals in vitro, and had good biocompatibility. (2) Compared with the control group, the apoptosis rate, reactive oxygen species, and malondialdehyde levels were increased (P < 0.05); the spread area of cells was decreased (P < 0.05), and the expression of collagen fiber I protein had no significant changes (P > 0.05) in the H2O2 group. Compared with the H2O2 group, reactive oxygen species level was decreased in the CMC-OCS group (P < 0.05), malondialdehyde level was decreased (P < 0.05), and cell spread area was increased (P <0.05) in the PRP group, CMC-OCS group, and CMC-OCS/PRP group; apoptosis rate was decreased in the CMC-OCS/PRP group (P < 0.05), and collagen fiber I protein expression was increased in the PRP group, CMC-OCS group, and CMC-OCS/PRP group (P < 0.05). (3) Compared with the control group, the number of cell migration was decreased (P < 0.05), and the migration area had no significant change (P > 0.05) in the H2O2 group. Compared with the H2O2 group, the number and area of cell migration were increased in the PRP group, CMC-OCS group, and CMC-OCS/PRP group (P < 0.05), and the increase was most significant in the CMC-OCS/PRP group. (4) Under oxidative stress, CMC-OCS/ PRP hydrogel can improve the migration ability of fibroblasts, resist cell apoptosis, and preserve cell extension function [ABSTRACT FROM AUTHOR]

BACKGROUND: Carnosic acid, a bioactive compound found in rosemary, has been shown to reduce inflammation and reactive oxygen species (ROS). However, its mechanism of action in osteoclast differentiation remains unclear. OBJECTIVE: To investigate the effects of carnosic acid on osteoclast activation, ROS production, and mitochondrial function. METHODS: Primary bone marrow-derived macrophages from mice were extracted and cultured in vitro. Different concentrations of carnosic acid (0, 10, 15, 20, 25 and 30 μmol/L) were tested for their effects on bone marrow-derived macrophage proliferation and toxicity using the cell counting kit-8 cell viability assay to determine a safe concentration. Bone marrow-derived macrophages were cultured in graded concentrations and induced by receptor activator of nuclear factor-κB ligand for osteoclast differentiation for 5-7 days. The effects of carnosic acid on osteoclast differentiation and function were then observed through tartrate-resistant acid phosphatase staining, F-actin staining, H2DCFDA probe and mitochondrial ROS, and Mito-Tracker fluorescence detection. Western blot and RT-PCR assays were subsequently conducted to examine the effects of carnosic acid on the upstream and downstream proteins of the receptor activator of nuclear factor-κB ligand-induced MAPK signaling pathway. RESULTS AND CONCLUSION: Tartrate-resistant acid phosphatase staining and F-actin staining showed that carnosic acid dose-dependently inhibited in vitro osteoclast differentiation and actin ring formation in the cell cytoskeleton, with the highest inhibitory effect observed in the high concentration group (30 μmol/L). Carnosic acid exhibited the most significant inhibitory effect during the early stages (days 1-3) of osteoclast differentiation compared to other intervention periods. Fluorescence imaging using the H2DCFDA probe, mitochondrial ROS, and Mito-Tracker demonstrated that carnosic acid inhibited cellular and mitochondrial ROS production while reducing mitochondrial membrane potential, thereby influencing mitochondrial function. The results of western blot and RT-PCR revealed that carnosic acid could suppress the expression of NFATc1, CTSK, MMP9, and C-fos proteins associated with osteoclast differentiation, and downregulate the expression of NFATc1, Atp6vod2, ACP5, CTSK, and C-fos genes related to osteoclast differentiation. Furthermore, carnosic acid enhanced the expression of antioxidant enzyme proteins and reduced the generation of ROS during the process of osteoclast differentiation. Overall, carnosic acid exerts its inhibitory effects on osteoclast differentiation by inhibiting the phosphorylation modification of the P38/ERK/JNK protein and activating the MAPK signaling pathway in bone marrow-derived macrophages. [ABSTRACT FROM AUTHOR]

BACKGROUND: Some studies have found that ferroptosis of osteoblasts can be an important mechanism to induce the occurrence and development of hormone-induced femoral head necrosis. With the development of Chinese medicine, some scholars have found that some Chinese medicine monomer, Chinese medicine compound and Chinese patent medicine can regulate the ferroptosis of osteoblasts through various pathway mechanisms, and finally play a role in the treatment of steroid-induced avascular necrosis of femoral head. OBJECTIVE: To investigate the relationship between ferroptosis and steroid-induced avascular necrosis of femoral head and the mechanism of Chinese medicine regulating ferroptosis of osteoblasts in the treatment of steroid-induced avascular necrosis of femoral head, so as to provide new ideas for the diagnosis and treatment of steroid-induced avascular necrosis of femoral head. METHODS: With “ferroptosis, steroid-induced avascular necrosis of femoral head, osteoblast, Chinese herbal medicine, glucocorticoid, iron metabolism, reactive oxygen species, glutathione peroxidase” as Chinese search terms, and “ferroptosis, hormonal necrosis of the femoral head, osteoblast, Chinese herbal medicine, glucocorticoid, iron metabolism, ROS, GPX4” as English search terms, the search was conducted on CNKI, PubMed, WanFang, VIP and other databases. The relevant articles on osteoblast ferroptosis and steroid-induced avascular necrosis of femoral head and the regulation of Chinese herbal medicine intervention from the establishment of each database to 2023 were screened. Finally, 76 articles were systematically analyzed. RESULTS AND CONCLUSION: (1) Ferroptosis of osteoblasts plays an important role in the pathogenesis of steroid-induced avascular necrosis of femoral head. (2) The occurrence of ferroptosis in osteoblasts is regulated by a variety of mechanisms, such as intracellular iron overload causing ferroptosis. Lipid peroxidation damages cell membrane and causes ferroptosis. Cystine/glutamate reverse transporter induced ferroptosis by influencing glutathione level and glutathione peroxidase 4 activity. Fenton reaction in the cell produces a large number of reactive oxygen species and causes ferroptosis. (3) Chinese medicine monomer icariin, Chinese medicine compound Qinge pills and Chinese patent medicine Bushen Huoxue granules can regulate the occurrence of osteoblast ferroptosis, and help to prevent and treat steroid-induced avascular necrosis of femoral head. (4) The mechanism of ferroptosis in osteoblasts is still unclear. Further investigation on the mechanism of action of both is expected to provide a new choice for clinical treatment of steroid-induced avascular necrosis of femoral head. [ABSTRACT FROM AUTHOR]

Objective To explore the inhibitory effect of daphnetin (Dap) on gastric cancer cells and its mechanism. Methods Gastric cancer AGS cells were treated with Dap at concentrations of 0, 30, 60, 90, 120, and 150 μmol/L, and the effect on cell viability was evaluated after 48 h using the MTT assay. AGS cells were divided into groups A to E, and each group was treated with Dap at concentrations of 0, 30, 60, 90, 120, and 150 μmol/L, respectively, for 48 h. Each group was observed for changes in cell count and morphology using optical microscopy and crystal violet staining. DCF staining was used to evaluate the effect of Dap on intracellular reactive oxygen species (ROS) levels in AGS cells in groups A to D, while JC-1 staining was used to evaluate the effect of Dap on the level of mitochondrial membrane potential (MMP) in AGS cells in groups A to D. Western blot was conducted to measure the expression levels of LC3 and P62 proteins in AGS cells in groups A to D, and changes in autophagic flux in AGS cells were measured by Ad-mCherry-GFP-LC3B staining. Results Dap significantly inhibited AGS cell viability in a concentration-dependent manner (F=321.50,t=12.44-34.77,P

BackgroundNatural pyrethrins have long been widely used in the fields of environmental and household hygiene. Studies have reported that natural pyrethrins have potential liver toxicity, but their specific mechanisms are still unclear yet. ObjectiveTo explore the effect of natural pyrethrins on DNA damage in human liver cells. MethodsThis study used human liver cell QSG7701 as an in vitro testing model. After exposure to DMSO and a series of concentrations of natural pyrethrins (5, 10, 20, and 40 μg·mL−1) for 6 and 24 h, reactive oxygen species (ROS) was detected by fluorescence microscopy using a fluorescence probe, thiobarbituric acid reactive substance (TBARS) by colorimetric method using a microplate reader, DNA damage by comet assay through observing DNA fragment migration under microscope, and phospho H2AX (γH2AX) and 8-oxoguanine (8-oxoG) by immunofluorescence assay using a laser confocal microscope. ResultsAs the exposure concentration of natural pyrethrins increased, the fluorescence intensity of ROS significantly increased in a concentration-dependent manner. The differences in ROS between the 10 μg·mL−1 and above groups and the control group were statistically significant (P

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BACKGROUND: Osteoporosis has a high incidence, leading to fracture and other complications. However, existing drugs have great side effects and are difficult to meet the clinical application. OBJECTIVE: To explore the effect and potential mechanism of fucoxanthin on osteoporosis induced by glucocorticoid. METHODS: Primary rat osteoblasts were inoculated in 6-well plates. When the cell fusion reached 80%, the cells were divided into four groups: the control group was cultured alone for 24 hours, the glucocorticoid group was intervened with dexamethasone for 24 hours, the fucoxanthin group was intervened with fucoxanthin for 24 hours, and the glucocorticoid + fucoxanthin group was intervened with dexamethasone and fucoxanthin at the same time for 24 hours. After intervention, cell proliferation, apoptosis, intracellular reactive oxygen species level, and protein expression of apoptosis-related proteins, bone formationrelated proteins, and nuclear factor erythroid-2-related factor 2 were detected. RESULTS AND CONCLUSION: Cell counting kit-8 results showed that the cell viability was decreased in the glucocorticoid group compared with the control group (P < 0.05) but increased in the glucocorticoid+fucoxanthin group compared with the glucocorticoid group (P < 0.05). JC-1 mitochondrial membrane potential staining and flow cytometry assay showed that the percentage of apoptosis increased in the glucocorticoid group compared with the control group (P < 0.05) but decreased in the glucocorticoid+fucoxanthin group compared with the glucocorticoid group (P < 0.05). Western blot assay showed that compared with the control group, the protein expression of BAX and cleaved poly (ADP-ribose) polymerase was elevated in the glucocorticoid group (P < 0.05), and the protein expression of BCL2, type I collagen α1 peptide chain, alkaline phosphatase, osteocalcin, and RUNX2 was decreased in the glucocorticoid group (P < 0.05). Compared with the glucocorticoid group, the protein expression of BAX and cleaved poly (ADP-ribose) polymerase was decreased (P < 0.05), and the protein expression of BCL2, type I collagen α1 peptide chain, alkaline phosphatase, osteocalcin, and RUNX2 was elevated (P < 0.05) in the glucocorticoid+fucoxanthin group. Fluorescent probe assay showed an increase in reactive oxygen species level in the glucocorticoid group compared with the control group (P < 0.05) and a decrease in reactive oxygen species level in the glucocorticoid+fucoxanthin group compared with the glucocorticoid group (P < 0.05). Immunofluorescence staining and western blot assay showed that the protein expression of nuclear factor erythroid-2-related factor 2 in the glucocorticoid group was decreased compared with that in the control group (P < 0.05); and the protein expression of nuclear factor erythroid-2-related factor 2 in the glucocorticoid+fucoxanthin group was elevated compared with that in the glucocorticoid group (P < 0.05). To conclude, fucoxanthin can improve glucocorticoid-induced osteoblast apoptosis and the expression of bone formation-related molecules by activating nuclear factor erythroid-2-related factor 2. [ABSTRACT FROM AUTHOR]

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Copyright of Shipin Kexue/ Food Science is the property of Food Science 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.)

Copyright of Shipin Kexue/ Food Science is the property of Food Science 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.)