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Cell volume as a characteristic of changes in response to external environmental cues has been shown to control the fate of stem cells. However, its influence on macrophage behavior and macrophage-mediated inflammatory responses have rarely been explored. Herein, through mediating the volume of macrophages by adding polyethylene glycol (PEG), we demonstrated the feasibility of fine-tuning cell volume to regulate macrophage polarization towards anti-inflammatory phenotypes, thereby enabling to reverse macrophage-mediated inflammation response. Specifically, lower the volume of primary macrophages can induce both resting macrophages (M0) and stimulated pro-inflammatory macrophages (M1) to up-regulate the expression of anti-inflammatory factors and down-regulate pro-inflammatory factors. Further mechanistic investigation revealed that macrophage polarization resulting from changing cell volume might be mediated by JAK/STAT signaling pathway evidenced by the transcription sequencing analysis. We further propose to apply this strategy for the treatment of arthritis via direct introduction of PEG into the joint cavity to modulate synovial macrophage-related inflammation. Our preliminary results verified the credibility and effectiveness of this treatment evidenced by the significant inhibition of cartilage destruction and synovitis at early stage. In general, our results suggest that cell volume can be a biophysical regulatory factor to control macrophage polarization and potentially medicate inflammatory response, thereby providing a potential facile and effective therapy for modulating macrophage mediated inflammatory responses. Cell volume has recently been recognized as a significantly important biophysical signal in regulating cellular functionalities and even steering cell fate. Herein, through mediating the volume of macrophages by adding polyethylene glycol (PEG), we demonstrated the feasibility of fine-tuning cell volume to induce M1 pro-inflammatory macrophages to polarize towards anti-inflammatory M2 phenotype, and this immunomodulatory effect may be mediated by the JAK/STAT signaling pathway. We also proposed the feasible applications of this PEG-induced volume regulation approach towards the treatment of osteoarthritis (OA), wherein our preliminary results implied an effective alleviation of early synovitis. Our study on macrophage polarization mediated by cell volume may open up new pathways for immune regulation through microenvironmental biophysical clues. [Display omitted] [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]

Objective: To investigate the effect and mechanism of Hippophae rhamnoides flavone (HRF) on polycystic ovarian syndrome (PCOS) in rats, and to provide new ideas for the prevention and treatment of PCOS. Methods: A PCOS rat model was duplicated by giving rats a high-fat diet combined with the intragastric administration of letrozole, and the model rats were randomly divided into model group, low-dose HRF group (200 mg/kg HRF), high-dose HRF group (400 mg/kg HRF) and metformin group (100 mg/kg). Changes in the related indicators were detected on the 21 d after the rats were administered with the different agents by gavage. Results: Compared with that in the model group, the ovarian index, the percentage of interestrus temporal image, the fasting blood glucose (FBG) level, the fasting insulin (FINS) content, the insulin resistance index (HOMA-IR), the activities of serum luteinizing hormone (LH) and testosterone (T), the levels of tumor necrosis factor α (TNF-α), interleukin 6 (IL-6) and C reactive protein (CRP) of rats in low- and high-dose HRF groups were respectively decreased significantly (P<0.05, P<0.01), while the activity of follicle stimulating hormone FSH) was significantly increased (P<0.01). The histopathological morphology of ovarian tissue of rats treated with the low and high doses of HRF was improved, and the expression levels of toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88) and nuclear factors-κBp65 (NF-κ Bp65) mRNAs as well as TLR4, MyD88 and p-NF-κBp65 proteins were significantly decreased (P<0.05, P<0.01). Conclusion: HRF could improve the symptoms of PCOS, alleviate the insulin resistance, regulate the level of sex hormones and repair the pathological changes in the ovarian tissue of rats with PCOS, and its mechanism may be related to its inhibition on the inflammatory response mediated by the TLR4/NF-κB signaling pathway. [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]

Pyruvate kinase M2 (PKM2) is a key rate-limiting enzyme in glycolysis. It is well known that PKM2 plays a vital role in the proliferation of tumor cells. However, PKM2 can also exert its biological functions by mediating multiple signaling pathways in neurological diseases, such as Alzheimer's disease (AD), cognitive dysfunction, ischemic stroke, post-stroke depression, cerebral small-vessel disease, hypoxic-ischemic encephalopathy, traumatic brain injury, spinal cord injury, Parkinson's disease (PD), epilepsy, neuropathic pain, and autoimmune diseases. In these diseases, PKM2 can exert various biological functions, including regulation of glycolysis, inflammatory responses, apoptosis, proliferation of cells, oxidative stress, mitochondrial dysfunction, or pathological autoimmune responses. Moreover, the complexity of PKM2's biological characteristics determines the diversity of its biological functions. However, the role of PKM2 is not entirely the same in different diseases or cells, which is related to its oligomerization, subcellular localization, and post-translational modifications. This article will focus on the biological characteristics of PKM2, the regulation of PKM2 expression, and the biological role of PKM2 in neurological diseases. With this review, we hope to have a better understanding of the molecular mechanisms of PKM2, which may help researchers develop therapeutic strategies in clinic. [ABSTRACT FROM AUTHOR]

Chronic sinusitis is a common inflammatory disease of the nasal and sinus mucosa, leading to symptoms such as nasal congestion, runny nose, decreased sense of smell, and headache. It often recurs and seriously affects the quality of life of patients. However, its pathological and physiological mechanisms are not fully understood. In recent years, the role of potassium ion channels in the regulation of mucosal barrier function and inflammatory cell function has received increasing attention. In chronic sinusitis, there are often changes in the expression and function of potassium channels, leading to mucosal damage and a stronger inflammatory response. However, the related research is still in its early stages. This article will review the role of the potassium channel in the pathological and physiological changes of chronic sinusitis. The studies revealed that BK/TREK-1 potassium channel play a protective role in the nasal mucosal function through p38-MAPK pathway, and KCa3.1/Kv1.3 enhance the inflammatory response of Chronic rhinosinusitis by regulating immune cell function, intracellular Ca2+ signaling and ERK/MAPK/NF-κB pathway. Because ion channels are surface proteins of cell membranes, they are easier to intervene with drugs, and the results of these studies may provide new effective targets for the prevention and treatment of chronic sinusitis. [ABSTRACT FROM AUTHOR]

Objective: To investigate the role of NEAT1 targeted regulation of miR‐125/ADAM9 mediated NF‐κB pathway in inflammatory response in rosacea. Method: HaCaT cell rosacea phenotype was induced by LL37. The connection targeted by NEAT1 and miR‐125a‐5p was confirmed by Double‐Luciferase report analysis. qPCR was employed to assess the levels of expression for NEAT1, miR‐125a‐5p, and ADAM9 genes. The levels of expression for ADAM9/TLR2/NF‐κB P65 pathway proteins in each batch of cells were determined by Western blotting. The levels of expression for inflammatory factors, including TNF‐α, IL‐1β, IL‐6, and IL‐18, were measured through ELISA experimentation. Results: LL37 could successfully induce HaCaT cells to exhibit rosacea phenotype. The luciferase report experiment confirmed that NEAT1 could target and bind miR‐125a‐5p and inhibit its expression. ADAM9 exhibited increased expression in LL37‐induced HaCaT cells, showing a positive association with NEAT1 expression and inverse relationship with miR‐125a‐5p activation. LL37 treatment promoted the expression of ADAM9/TLR2/NF‐κB P65 pathway proteins. Silencing ADAM9 can inhibit the inflammatory signaling pathway and reduce the level of TNF‐α, IL‐1β, IL‐6, and IL‐18 in HaCaT cells. Conclusion: NEAT1 can suppress the production of miR‐125a‐5p and activate the TLR2/NF‐κB inflammatory pathway mediated by ADAM9, thereby promoting the inflammatory response in rosacea. [ABSTRACT FROM AUTHOR]

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Objective: To investigate the effect and mechanism of Hippophae rhamnoides flavone (HRF) on polycystic ovarian syndrome (PCOS) in rats, and to provide new ideas for the prevention and treatment of PCOS. Methods: A PCOS rat model was duplicated by giving rats a high-fat diet combined with the intragastric administration of letrozole, and the model rats were randomly divided into model group, low-dose HRF group (200 mg/kg HRF), high-dose HRF group (400 mg/kg HRF) and metformin group (100 mg/kg). Changes in the related indicators were detected on the 21 d after the rats were administered with the different agents by gavage. Results: Compared with that in the model group, the ovarian index, the percentage of interestrus temporal image, the fasting blood glucose (FBG) level, the fasting insulin (FINS) content, the insulin resistance index (HOMA-IR), the activities of serum luteinizing hormone (LH) and testosterone (T), the levels of tumor necrosis factor α (TNF-α), interleukin 6 (IL-6) and C reactive protein (CRP) of rats in low- and high-dose HRF groups were respectively decreased significantly (P

Vernal keratoconjunctivitis is an allergic ocular surface disease mostly present with recurrent chronic inflammation, which usually affects children and adolescents and possibly results in corneal complications such as keratoconus. Keratoconus is a corneal disease characterized by a local cone-like corneal deformation. Previous studies have respectively put forward pathological mechanisms of vernal keratoconjunctivitis and keratoconus and the progressive risk factors, among which we find there's mutual mechanisms as well as cytokines' expression, including type I and IV hypersensitivity, inflammatory reaction, enzymatic changes, oxidative stress and mechanical injury. This review aims at summarizing the possible intrinsic mechanisms and cytokines exacerbating vernal keratoconjunctivitis patients corneas to keratoconus, so as to provide reference for the prevention and management in keratoconus caused by vernal keratoconjunctivitis.

Context Diabetic peripheral neuropathy (DPN) results in an enormous burden and reduces the quality of life for patients. Considering there is no specific drug for the management of DPN, traditional Chinese medicine (TCM) has increasingly drawn attention of clinicians and researchers around the world due to its characteristics of multiple targets, active components, and exemplary safety.Objective To summarize the current status of TCM in the treatment of DPN and provide directions for novel drug development, the clinical effects and potential mechanisms of TCM used in treating DPN were comprehensively reviewed.Methods Existing evidence on TCM interventions for DPN was screened from databases such as PubMed, the Cochrane Neuromuscular Disease Group Specialized Register (CENTRAL), and the Chinese National Knowledge Infrastructure Database (CNKI). The focus was on summarizing and analyzing representative preclinical and clinical TCM studies published before 2023.Results This review identified the ameliorative effects of about 22 single herbal extracts, more than 30 herbal compound prescriptions, and four Chinese patent medicines on DPN in preclinical and clinical research. The latest advances in the mechanism highlight that TCM exerts its beneficial effects on DPN by inhibiting inflammation, oxidative stress and apoptosis, endoplasmic reticulum stress and improving mitochondrial function.Conclusions TCM has shown the power latent capacity in treating DPN. It is proposed that more large-scale and multi-center randomized controlled clinical trials and fundamental experiments should be conducted to further verify these findings.

Background/purpose: The handheld nonthermal plasma (HNP) treatment may alter the surface properties, bone metabolism, and inflammatory reactions of polyaryletherketone (PAEK) dental implant materials. This study tested whether the HNP treatment might increase the biocompatibility, surface hydrophilicity, surface free energies (SFEs), and the cell adhesion and mineralization capability of PAEK materials. Materials and methods: Disk-shaped samples of titanium (Ti), zirconia (Zr), polyetheretherketone (PEEK [PE]), and polyetherketoneketone (PEKK [PK]) were subjected to HNP treatment and termed as TiPL, ZrPL, PEPL, and PKPL, respectively. Water-surface reactions were examined using a goniometer. MG-63 cells were cultured on all samples to assess the cell viability, cytotoxicity, cell attachment, and mineralization characteristics. The expression of pro-inflammatory cytokines (tumor necrosis factor-alpha and interleukin-6) and key mineralization markers (alkaline phosphatase [ALKP], osteopontin [OPN], and dentin matrix protein 1 [DMP1]) was measured using enzyme-linked immunosorbent assay kits. Results: The HNP-treated samples exhibited significantly enhanced surface hydrophilicities and SFEs compared to the untreated samples. The cell viability remained high across all samples, indicating no cytotoxic effects. The HNP treatment significantly enhanced MG-63 cell adherence and proliferation. Elevated levels of ALKP and OPN were observed for the plasma-treated PEPL and PKPL specimens, while DMP1 levels increased significantly only in the PKPL specimen. Pro-inflammatory cytokine levels were low across all samples, suggesting no inflammatory response. Conclusion: The HNP-treated PAEKs have enhanced the surface hydrophilicity and SFEs as well as superior cell adhesion and mineralization capability, and thus may be good clinical dental implant materials.

Diabetic kidney disease (DKD) is a serious complication of diabetes mellitus (DM) and has become the main cause of end-stage renal disease worldwide. In recent years, with the increasing incidence of DM, the pathogenesis of DKD has received increasing attention. The pathogenesis of DKD is diverse and complex. Extracellular vesicles (EVs) contain cell-derived membrane proteins, nucleic acids (such as DNA and RNA) and other important cellular components and are involved in intercellular information and substance transmission. In recent years, an increasing number of studies have confirmed that EVs play an important role in the development of DKD. The purpose of this paper is to explain the potential diagnostic value of EVs in DKD, analyze the mechanism by which EVs participate in intercellular communication, and explore whether EVs may become drug carriers for targeted therapy to provide a reference for promoting the implementation and application of exosome therapy strategies in clinical practice. [ABSTRACT FROM AUTHOR]

Ischemic stroke is a common acute cerebrovascular disease in clinical practice， which poses a severe threat to human health. In recent years， with deepening understanding of ischemic stroke， significant progress has been made in the diagnosis and treatment. However， current treatments for ischemic stroke are partially limited due to extremely complex pathological mechanisms. Studies have shown that mitochondrial dysfunction plays an important role in the pathogenesis of ischemic stroke. Therefore， modulation of mitochondrial function through mitochondrial dynamics is essential to ameliorate the damage of cerebral ischemic neuronal cells. In this article， the molecular mechanism of mitochondrial dynamics and its role in ischemic stroke were reviewed， aiming to provide useful reference for the treatment of ischemic stroke.

Background. In recent years, a wider range of bakery products with a lower glycaemic response can be observed in the food industry. This contributes to the provision of a wider range of cereal bakery products. The gradual increase in the consumption of brown bread is significant, but despite this, white bread remains a part of the typical Western diet. Studies showed high intake of carbohydrates increase TG levels by enhancing hepatic synthesis of very low-density lipoprotein (VLDL) and decrease activity of lipoprotein lipase. White bread consumption has been therefore associated with an unhealthy lifestyle. Objective. The aim of this study was to assess the influence of the consumption of gluten bakery products on lipids and inflammatory parameters of the probands. Material and Methods. The monitored group consisted of 30 probands from the general population. The average age of the monitored group was 29.7 years. The intervention dose consisted of a different combination of several types of bakery products containing gluten (bread, pastries, soft pastries) within the individual weeks of consumption, while the intervention lasted 6 weeks. An intervention dose of 150 to 200 g per day was set for women and 200 to 250 g per day for men. Biochemical blood parameters were determined using a fully automatic Biolis 24i Premium blood serum biochemical analyzer, by end-point photometry method. We tested the differences between the biochemic parameters by one-factor analysis of variance (ANOVA) and compared them by Tuckey’s Post Hoc Test. Results. The measurement of the lipid profile showed that the average levels of total cholesterol (TC) were above the reference value (

Objective To observe the cell viability, pyroptosis, inflammation and oxidative stress response of the preeclampsia (Preeclampsia, PE) model cells constructed using the human chorionic trophoblast cell line HTR-8/SVneo with low expression of microRNA-148a (miR-148a). Methods Human chorionic trophoblast cell line HTR-8/SVneo in the logarithmic growth phase were selected and divided into groups A, B, C, and D. Cells in the group A were transfected with miR-148a inhibitor (inhibiting miR-148a expression) for 24 h, followed by the addition of 100 ng/L LPS for 24 h (establishing a PE model cell); cells in the group B were transfected with NC inhibitor (blank control) and cultured for 24 h, followed by the addition of 100 ng/L LPS for 24 h; cells in the group C were cultured with 100 ng/L LPS for 24 h; cells in the group D were not treated. At 48 h of culture, qRT-PCR was used to detect miR-148a in cells of each group; CCK-8 was used to detect cell viability in each group; TUNEL method was used to calculate the apoptosis rate in each group; Western blotting was used to detect the apoptosis-related proteins Caspase-1, GSDMD, and NLRP3 in each group; ELISA was used to detect inflammatory factors (tumor necrosis factor-a [TNF-a], interleukin-1B [IL-1B], IL-6) and oxidative stress indicators (glutathione peroxidase [GSH], superoxide dismutase [SOD], and malondialdehyde [MDA]) in the supernatant of each group. Results Compared with the group D, the relative expression level of miR-148a was higher, and the OD values were lower at 24, 48, and 72 h of culture, the apoptosis rate was higher, and the relative expression levels of Caspase-1, GSDMD, and NLRP3 proteins in cells were higher in the group C (all P<0.05). Compared with the group B, the relative expression level of miR-148a was lower, and the OD values were higher at 24, 48, and 72 h of culture, the apoptosis rate was lower, and the relative expression levels of Caspase-1, GSDMD, and NLRP3 proteins in cells were low- er in the group A (all P<0.05). Compared with the group D, the levels of TNF-a, IL-1B, and IL-6 in the cell supernatant increased, the expression levels of GSH and SOD in cells were lower, while the expression of MDA increased in the group C (all P<0.05). Compared with the group B, the levels of TNF-a, IL-1B, and IL-6 in the cell supernatant were lower, the expression levels of GSH and SOD increased, and the expression of MDA decreased in the group A (all P<0.05). Conclusions The cell viability of the PE model cells constructed using HTR-8/SVneo with low expression of miR-148a is high, while the degree of pyroptosis, inflammatory response and oxidative stress response are low. MiR-148a may be one of the therapeutic targets of PE. [ABSTRACT FROM AUTHOR]

To explore the expression of inflammatory factors and TSP-1 in gingival crevicular fluid in patients undergoing orthodontic extraction, and the influencing factors of periodontal disease. Eighty patients admitted to our hospital from August 2020 to August 2023 for orthodontic treatment of extracted teeth were retrospectively analyzed, and gingival sulcus fluid samples were taken from all the patients before orthodontic treatment, 1 month after orthodontic treatment, 3 months after orthodontic treatment, and at the end of orthodontic treatment to detect the tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), interleukin-6 (IL-6), and platelet reactive protein- 1 (TSP-1) expression levels. Subsequently, the patients were divided into periodontal disease group (n=36) and non-periodontal disease group (n=44) according to whether they suffered from periodontal disease during orthodontic treatment, compared the expression levels of TNF-琢, IL-1茁, IL-6, and TSP-1 of the patients in the two groups before orthodontic treatment and at the end of orthodontic treatment, and compared the general conditions of the patients in the two groups, and then analyzed the influence factors of periodontal diseases in patients with extracted teeth in orthodontics with the use of logistic regression model. Disease Influencing Factors. TNF-琢, IL-1茁, IL-6, and TSP-1 levels were elevated at 1 month and 3 months after orthodontic treatment in 80 patients with extracted teeth, and TNF-琢, IL-1茁, IL-6, and TSP-1 levels leveled off from 3 months to the end of orthodontic treatment, but were significantly higher than those before orthodontic treatment at 1 month, 3 months, and at the end of orthodontic treatment (P<0.05); there were significant differences in the expression levels of TNF-琢, IL-1茁, IL-6, and TSP-1 in patients in the periodontal diseases group compared to those in the non periodontal diseases group, and the expression levels in the periodontal diseases group were significantly higher than those in the non periodontal diseases group (P<0.05). There were significant differences in the expression levels of TNF-琢, IL-1茁, IL-6, and TSP-1 between patients in the pre-orthodontic and post-orthodontic groups, and the periodontal disease group was significantly higher than the non-periodontal disease group (P<0.05); there were no significant differences in the comparison of gender, age, and BMI between patients in the periodontal disease group and the non-periodontal disease group (P>0.05), and there were no significant differences in the duration of orthodontic treatment, number of extractions, oral cavity, oral cavity, and oral health of patients in the periodontal disease group and the non-periodontal disease group (P<0.05). number, orthodontic method, and oral cleanliness were compared significantly (P<0.05); logistic regression analysis showed that TNF-琢, IL-1茁, IL-6, TSP-1, orthodontic method, and oral cleanliness were independent risk factors for periodontal disease in patients with extracted teeth and orthodontic treatment (P<0.05). Inflammatory factors of gingival crevicular fluid and TSP-1 levels increased significantly in orthodontic patients with prolonged orthodontic time, and TNF-琢, IL-1 茁, IL-6, TSP-1, orthodontic mode and oral cleanliness were independent risk factors for periodontal disease in orthodontic patients. [ABSTRACT FROM AUTHOR]

Aim: To evaluate the inflammatory reaction and the ability to induce mineralization activity of a new repair material, NeoPUTTY (NPutty; NuSmile, USA), in comparison with Bio‐C Repair (BC; Angelus, Brazil) and MTA Repair HP (MTA HP; Angelus, Brazil). Methodology: Polyethylene tubes were filled with materials or kept empty (control group, CG) and implanted in subcutaneous tissue of rats for 7, 15, 30, and 60 days (n = 6/group). Capsule thickness, number of inflammatory cells (ICs), fibroblasts, collagen content, and von Kossa analysis were performed. Unstained sections were evaluated under polarized light and by immunohistochemistry for osteocalcin (OCN). Data were submitted to two‐way anova followed by Tukey's test (p ≤.05), except for OCN. OCN data were submitted to Kruskal–Wallis and Dunn and Friedman post hoc tests followed by the Nemenyi test at a significance level of 5%. Results: At 7, 15, and 30 days, thick capsules containing numerous ICs were seen around the materials. At 60 days, a moderate inflammatory reaction was observed for NPutty, BC while MTA HP presented thin capsules with moderate inflammatory cells. In all periods, NPutty specimens contained the highest values of ICs (p <.05). From 7 to 60 days, the number of ICs reduced significantly while an increase in the number of fibroblasts and birefringent collagen content was observed. At 7 and 15 days, no significant difference was observed in the immunoexpression of OCN (p >.05). At 30 and 60 days, NPutty showed the lowest values of OCN (p <.05). At 60 days, a similar immunoexpression was observed for BC and MTA HP (p >.05). In all time intervals, capsules around NPutty, BC, and MTA HP showed von Kossa‐positive and birefringent structures. Conclusions: Despite the greater inflammatory reaction promoted by NeoPutty than BC and MTA HP, the reduction in the thickness of capsules, the increase in the number of fibroblasts, and the reduction in the number of ICs indicate that this bioceramic material is biocompatible Furthermore, NeoPutty presents the ability to induce mineralization activity. [ABSTRACT FROM AUTHOR]

The purpose of this paper was to investigate the anti-inflammatory and anti-angiogenic activities of sulfated polysaccharide from C. tomentosum (PCT) using carrageenan (CARR)-induced paw edema in a rat model and anti-vasculogenic activity on a chorioallantoic membrane assay (CAM) model. Based on in vitro tests of anti-radical, total antioxidant, and reducing power activities, PCT presents a real interest via its antioxidant activity and ability to scavenge radical species. The in vivo pharmacological tests suggest that PCT possesses anti-inflammatory action by reducing paw edema and leukocyte migration, maintaining the redox equilibrium, and stabilizing the cellular level of several pro-/antioxidant system markers. It could significantly decrease the malondialdehyde levels and increase superoxide dismutase, glutathione peroxidase, and glutathione activities in local paw edema and erythrocytes during the acute inflammatory reaction of CARR. PCT pretreatment was effective against DNA alterations in the blood lymphocytes of inflamed rats and reduced the hematological alteration by restoring blood parameters to normal levels. The anti-angiogenic activity results revealed that CAM neovascularization, defined as the formation of new vessel numbers and branching patterns, was decreased by PCT in a dose-dependent manner, which supported the in silico bioavailability and pharmacokinetic findings. These results indicated the therapeutic effects of polysaccharides from C. tomentosum and their possible use as anti-proliferative molecules based on their antioxidant, anti-inflammatory, and anti-angiogenic activities. [ABSTRACT FROM AUTHOR]

Objective To explore the clinical efficacy of acetylcysteine solution retained perfusion inhalation treatment under electronic bronchoscopy in children with severe bacterial pneumonia. Methods From January 1，2021 to December 31，2022，86 children with severe bacterial pneumonia treated in the Department of Respiratory Medicine of Kunming Children’s Hospital were randomly divided into a control group (n = 43) and a study group (n = 43) . The children in the control group received electronic bronchoscopy under physiological saline pulmonary alveolar lavage treatment. The study group received acetylcysteine solution treatment retained after the end of the pulmonary lavage treatment. The clinical treatment effects， inflammatory indicators， tidal breathing function，and adverse reactions of the two groups were compared. Results After treatment，compared with control group，the hospitalization time，cough disappearance time and comorbidities disappearance time of children in study group were significantly shortened (P < 0.05), and the total effective rate of study group was significantly higher than that of control group (P < 0.05) . The levels of white blood cell count，procalcitonin，C-reactive protein， interleukin-6，and tumor necrosis factor-α of study group were significantly lower than those of control group (P < 0.05) . The tidal volume per kilogram of body weight，peak time ratio，and peak volume ratio levels of study group were significantly higher than those of control group (P < 0.05) .There was no statistically significant difference in the adverse drug reactions between two groups （P > 0.05）. Conclusion Under electronic bronchoscopy，preserving perfusion and inhaling acetylcysteine solution can significantly improve the clinical symptoms， inflammatory indicators，and lung function of children with severe bacterial pneumonia，and it is relatively safe [ABSTRACT FROM AUTHOR]

Sevoflurane exposure can result in neurotoxicity especially among children, which remains an important complication after surgery. However, its related mechanisms remain unclear. Here, we investigated the biological roles of SHARPIN in sevoflurane-induced neurotoxicity. As detected by qPCR, Western blotting and immunohistochemical staining, SHARPIN and HMGB1 expression was elevated in sevoflurane-stimulated mice as compared with the control mice. SHARPIN depletion attenuated hippocampus injury, repressed the expression of HMGB1 and M1-like macrophage markers (iNOS, TNF-α, IL-1β, IL-6), but enhanced the expression of M2-like macrophage markers (ARG-1, IL-10). GST pull-down and Co-IP assays demonstrated that SHARPIN directly interacted with HMGB1 to enhance HMGB1 expression in SH-SY5Y cells. The inhibitory effects of SHARPIN silencing on inflammatory reaction and M1-like macrophages were counteracted by HMGB1 overexpression. Finally, SHARPIN-HMGB1 pathway affected neuroinflammation triggered by sevoflurane via modulating macrophage polarization. Collectively, our data suggested that SHARPIN stimulated sevoflurane-induced neurotoxicity via converting M2-like macrophages to M1-like macrophages by enhancing HMGB1 expression. SHARPIN intervention may be a promising therapeutic method to relieve sevoflurane-induced neurotoxicity. [ABSTRACT FROM AUTHOR]

Background: This study investigated the contact between adult dental pulp stem cells (DPSCs) and carbamide peroxide (CP), a bleaching agent that is a popular choice for at-home whitening products, using an in vitro model. Objectives: The aim of this study was to evaluate the impact of exposure to different concentrations and timings of a commonly used peroxide-based home tooth-whitening product on DPSCs. Materials and methods: Human DPSCs obtained from impacted third molars were cultured and exposed to various concentrations of carbamide peroxide (0.1%, 0.5%, and 1%). The effects of CP on DPSC proliferation and apoptosis were investigated by MTT assay and flow cytometry. Migration was investigated by micrographs of wound healing. An enzyme-linked immunosorbent assay (IL-6 and IL-8) was used to investigate the CP-stimulated cytokine production of DPSCs. Each experiment was performed three times with independent batches of DPSCs. Statistical analysis of the collected data was performed using one-way and two-way ANOVAs with the significance threshold set at p < 0.05. Tukey's post hoc multiple comparison test was used to identify differences between groups. Results: Cell viability and adherence were lower in the CP-exposed cells compared to the non-stimulated cells, probably due to increased cell death (** p ≤ 0.01, **** p ≤ 0.0001). CP-stimulated DPSCs exhibited a dose-dependent release of IL-6 and IL-8 (**** p ≤ 0.0001). CP did not affect wound healing at any concentration tested. Conclusions: Human DPSCs were able to sense CP. Consequently, CP contributed significantly to cell apoptosis and local inflammatory responses through cytokine release. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD), the most common form of dementia, has a complex pathogenesis. The number of AD patients has increased in recent years due to population aging, while a trend toward a younger age of onset has arisen, imposing a substantial burden on society and families, and garnering extensive attention. DNA methylation has recently been revealed to play an important role in AD onset and progression. DNA methylation is a critical mechanism regulating gene expression, and alterations in this mechanism dysregulate gene expression and disrupt important pathways, including oxidative stress responses, inflammatory reactions, and protein degradation processes, eventually resulting in disease. Studies have revealed widespread changes in AD patients' DNA methylation in the peripheral blood and brain tissues, affecting multiple signaling pathways and severely impacting neuronal cell and synaptic functions. This review summarizes the role of DNA methylation in the pathogenesis of AD, aiming to provide a theoretical basis for its early prevention and treatment. [ABSTRACT FROM AUTHOR]

Abdominal aortic aneurysm (AAA) is a common disease in the elderly, with an increasing incidence rate, easy rupture, high mortality, and no effective drugs to slow down the development of AAA. The pathogenesis of AAA is closely related to extracellular matrix degradation, apoptosis of vascular smooth muscle cells and inflammation. It has been found that arachidonic acid derivatives, especially prostaglandins such as prostaglandin E2 (PGE2), prostaglandin D2 (PGD2) and thromboxane A2(TXA2), play important roles in the development of AAA. Therefore, this review discusses the mechanism of arachidonic acid derivatives in the development of AAA, as well as the latest research progress of the drugs, to provide ideas for the treatment of AAA and the discovery of new drug targets. [ABSTRACT FROM AUTHOR]

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.)

Canine visceral leishmaniasis (CVL), caused by the protozoan Leishmania infantum, affects several organs, including the skin. Dogs are considered the major domestic reservoir animals for leishmaniasis, and through their highly parasitized skin, they can serve as a source of infection for sandfly vectors. Therefore, studies of the skin parasite–host relationship can contribute to the understanding of the infectious dissemination processes of parasites in the dermis and help to identify targets for diagnosis and treatment. Thus, the aim of this study was to evaluate the association of anatomical vascular differences and Leishmania-induced vascular morphological changes with clinical signs and parasite load by analyzing the ear and abdominal skin from dogs naturally infected with L. infantum. Paired samples of ear and abdominal skin from L. infantum-positive dogs (n = 26) were submitted for histological and immunohistochemistry analyses. The ear skin samples showed a more intense and more diffusely distributed granulomatous inflammatory reaction, a higher number and larger diameter of blood vessels, increased parasite load, higher expression of VEGF+ (vascular endothelial growth factor) and MAC 387+ (calprotectin) recently infiltrating cells, and more intense collagen disruption compared to the abdominal skin samples. Intracellular amastigotes were observed in blood vessels and inside endothelial cells and were diffusely distributed throughout the dermis in the ear skin samples. The NOS2/MAC387+ cell ratio was lower in the ear skin samples than in those of the abdomen, suggesting that in the ear dermis, the inflammatory infiltrate was less capable of producing NO and thereby control the parasite load. Together, these findings indicate how parasites and immune cells are distributed in the skin and suggest an important role for dermal vascularization in cellular influx and thereby in parasite dissemination through the skin of naturally infected dogs. [ABSTRACT FROM AUTHOR]

Ischemic stroke is a common acute cerebrovascular disease in clinical practice, which poses a severe threat to human health. In recent years, with deepening understanding of ischemic stroke, significant progress has been made in the diagnosis and treatment. However, current treatments for ischemic stroke are partially limited due to extremely complex pathological mechanisms. Studies have shown that mitochondrial dysfunction plays an important role in the pathogenesis of ischemic stroke. Therefore, modulation of mitochondrial function through mitochondrial dynamics is essential to ameliorate the damage of cerebral ischemic neuronal cells. In this article, the molecular mechanism of mitochondrial dynamics and its role in ischemic stroke were reviewed, aiming to provide useful reference for the treatment of ischemic stroke. [ABSTRACT FROM AUTHOR]

Objective To investigate the effects of L-carnitine supplementation in uremic patients receiving hemodialysis. Methods Totally100 uremic patients undergoing hemodialysis were randomly divided into the control group and observation group according to the random number table, with 50 cases in each group. All patients received hemodialysis and routine nursing management, and patients in the observation group received intravenous drip of L-carnitine after hemodialysis treatment. The clinical effect of the hemodialysis treatment was evaluated, and changes of renal function indexes, nutrition indexes, serum inflammatory factors and complications were compared between two groups. Results The overall effective rate was 98. 00%(49/50)in the observation group and 86. 00%(43/50)in the control group, with no significant difference (P＞0. 05). Compared with patients in the controlgroup, patients in the observation group had a higher Ccr and lower level of Scr and BUN after treatment(P＜0. 05). The levels of PA, TRF, ALB and Hb in the observation group were higher than those in the control group after treatment(P＜0. 05). The levels of IL-6, CRP and TNF-α in the observation group were lower than those in the control group after treatment(P＜0. 05). There was no significant difference in incidence of complication between two groups(P＞0. 05). Conclusion The application of L-carnitine in hemodialysis treatment for uremic patients can improve the renal function and nutritional status, reduce the inflammatory reaction and complications, and helps to ensure the efficacy of hemodialysis treatment (目的 探讨左卡尼汀对尿毒症血液透析患者营养指标及炎症状态的影响。方法 选取2019年1月—2021年6月医院收治的尿毒症患者100例, 采用随机数字表法分为对照组和观察组, 各50例。两组均实施常规血液透析治疗和护理, 观察组于每次静脉透析治疗后静脉滴注左卡尼汀。评价两组治疗效果, 对比两组肾功能指标、营养指标、血清炎性因子指标、并发症发生情况。结果 观察组总有效率为98. 00%(49/50), 高于对照组的86. 00%(43/50), 差异无统计学意义(P＞0. 05)。治疗后, 观察组内生肌酐清除率(Ccr)高于对照组, 血肌酐(Scr)和尿素氮(BUN)水平低于对照组, 差异有统计学意义(P＜0. 05)。治疗后, 观察组前清蛋白(PA)、转铁蛋白(TRF)、白蛋白(ALB)、血红蛋白 (Hb)水平高于对照组, 差异有统计学意义(P＜0. 05)。治疗后, 观察组白细胞介素-6(IL-6)、C反应蛋白(CRP)和肿瘤坏死因子-α(TNF-α)水平低于对照组, 差异有统计学意义(P＜0. 05)。两组并发生发生率差异无统计学意义(P＞0. 05)。结论 尿毒症患者血液透析治疗中应用左卡尼汀, 能改善患者营养状况, 减轻炎症反应, 降低并发症风险, 确保透析治疗效果。)

Tianrui Zhang,1,&ast; Sha Fu,1,&ast; Xiaofeng Cao,2 Yangjingyi Xia,1 Manyan Hu,1 Qinghua Feng,1 Yujun Cong,1 Yuan Zhu,1 Xiaogang Tang,1 Minghua Wu1 1Department of Neurology, Affiliated Hospital of Nanjing University of Chinese Medicine, Jiangsu Province Hospital of Chinese Medicine, Nanjing, 210029, People’s Republic of China; 2Department of Neurology, Jiangyan Hospital of Chinese Medicine, Taizhou, Jiangsu, 225500, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Minghua Wu; Xiaogang Tang, Department of Neurology, Affiliated Hospital of Nanjing University of Chinese Medicine, 155 Hanzhong Road, Nanjing, 210029, People’s Republic of China, Tel +8613951786719, Email yfy0069@njucm.edu.cn; zhongyiTXG@163.comPurpose: According to many previous studies, neutrophil-to-lymphocyte ratio (NLR), lymphocyte-to-monocyte ratio (LMR) and hypersensitive C-reactive protein (CRP) are commonly used as important indicators to assess the prognosis of intravenous thrombolysis in AIS patients. Based on this, we used two novel biomarkers C-NLR (CRP/neutrophil-to-lymphocyte ratio) and C-LMR (CRP×lymphocyte-to-monocyte ratio) to investigate their correlation with 90-day outcomes in AIS patients after intravenous thrombolysis.Patients and Methods: A total of 204 AIS patients who received intravenous thrombolysis at the Stroke Center of Jiangsu Province Hospital of Chinese Medicine from January 2021 to December 2022 were retrospectively included. All patients were followed up 90 days after thrombolysis to assess their prognosis. Patients with a modified Rankin scale score (mRS) of 3– 6 were included in the unfavorable outcome group, and those with a score of 0– 2 were included in the favorable outcome group. Logistic regression analysis, receiver operating characteristic (ROC) curve, and Kaplan–Meier survival curve were used to investigate the association between C-NLR, C-LMR, and 90-day prognosis in AIS patients treated with early intravenous thrombolysis.Results: C-NLR (OR=1.586, 95% CI=1.098~2.291, P=0.014) and C-LMR (OR=1.099, 95% CI=1.025~1.179, P=0.008) were independent risk factors for 90-day prognosis of AIS patients treated with early intravenous thrombolysis. The higher C-NLR and C-LMR were associated with unfavorable prognosis.Conclusion: C-NLR and C-LMR can be used as biomarkers to predict prognosis of AIS patients treated with early intravenous thrombolysis.Keywords: modified rankin scale, reperfusion therapy, inflammatory reaction, cerebral vascular disease, clinical prognosis

Objective: To investigate the protective effect of garlic polysaccharides against metabolic-associated fatty liver disease (MAFLD) in mice. Methods: Totally 50 male C57BL/6 mice were randomly equally divided into five groups, namely, normal, model, low-, medium-, and high-dose garlic polysaccharides (250, 1 000, and 3 000 mg/kg mb, respectively). After 28 days of feeding, serum and liver samples were taken for pathomorphological examination, biochemical assays, and quantitative analysis of the expression of the genes Hmox1, Cat, Gpx1, Tnf, Ccl2, Cxcl2, Cxcl10, IL-1a, IL-1b, Fasn, Acaca, Cpt1a, Acox, Cd36, Fabp1, Apob and Mttp. Results: Compared with the model group, garlic polysaccharides at the medium and high doses significantly alleviated MAFLD, restoring the pathological morphology to normal, bringing the levels of malondialdehyde (MDA) and superoxide dismutase (SOD) in liver tissue back to near-normal levels, and obviously restoring the expression of Hmox1, Tnf, Ccl2, Cxcl2, Cxcl10, Cpt1a, and Acox to normal levels. Conclusion: Intervention of garlic polysaccharides, especially at the medium dose, can basically eliminate liver damage caused by MAFLD. The underlying mechanism may be related to the regulation of lipid metabolism and inflammatory gene expression through suppressing the nuclear factor-κB signaling pathway, thereby reducing lipid deposition and lipid peroxidation.

Macrophages play a central role in immunological responses to metallic species associated with the localized corrosion of metallic implants, and mediating in peri-implant inflammations. Herein, the pathways of localized corrosion-macrophage interactions were systematically investigated on 316L stainless steel (SS) implant metals. Electrochemical monitoring under macrophage-mediated inflammatory conditions showed a decreased pitting corrosion resistance of 316L SSs in the presence of RAW264.7 cells as the cells would disrupt biomolecule adsorbed layer on the metal surface. The pitting potentials were furtherly decreased when the RAW264.7 cells were induced to the M1 pro-inflammatory phenotype by the addition of lipopolysaccharide (LPS), and pitting corrosion preferentially initiated at the peripheries of macrophages. The overproduction of aggressive ROS under inflammatory conditions would accelerate the localized corrosion of 316L SS around macrophages. Under pitting corrosion condition, the viability and pro-inflammatory polarization of RAW264.7 cells were region-dependent, lower viability and more remarkable morphology transformation of macrophages in the pitting corrosion region than the pitting-free region. The pitting corrosion of 316L SS induced high expression of CD86, TNF-α, IL-6 and high level of intracellular ROS in macrophages. Uneven release of metallic species (Fe2+, Cr3+, Ni2+, etc) and uneven distribution of surface overpotential stimulated macrophage inflammatory responses near the corrosion pits. A synergetic effect of localized corrosion and macrophages was revealed, which could furtherly promote localized corrosion of 316L SS and macrophage inflammatory reactions. Our results provided direct evidence of corrosion-macrophage interaction in metallic implants and disclosed the pathways of this mutual stimulation effect.

Diabetic kidney disease (DKD) is a serious complication of diabetes mellitus (DM) and has become the main cause of end-stage renal disease worldwide. In recent years, with the increasing incidence of DM, the pathogenesis of DKD has received increasing attention. The pathogenesis of DKD is diverse and complex. Extracellular vesicles (EVs) contain cell-derived membrane proteins, nucleic acids (such as DNA and RNA) and other important cellular components and are involved in intercellular information and substance transmission. In recent years, an increasing number of studies have confirmed that EVs play an important role in the development of DKD. The purpose of this paper is to explain the potential diagnostic value of EVs in DKD, analyze the mechanism by which EVs participate in intercellular communication, and explore whether EVs may become drug carriers for targeted therapy to provide a reference for promoting the implementation and application of exosome therapy strategies in clinical practice.

Copyright of Traditional Chinese Drug Research & Clinical Pharmacology is the property of Traditional Chinese Drug Research & Clinical Pharmacology 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 probe into the effects of Baihe Liyan capsules on swallowing function, immunity and analgesia in patients with acute laryngopharyngitis of lung-stomach excess-heat syndrome. METHODS: A total of 260 patients with acute laryngopharyngitis admitted into the hospital from 2021 to 2022 were selected to be divided into control group and observation group via random number table method. The 130 cases (7 cases withdraw, 123 cases actually enrolled) in the control group were given conventional treatment, and 130 cases (5 cases withdraw, 125 cases actually enrolled) in the Baihe Liyan capsules group were given Baihe Liyan capsules based on the control group. The vascular cell adhesion molecule (VCAM-1), hypersensitivity C reaction protein (hs-CRP), secreted immunoglobulin A (SIgA), interleukin 1β (IL-1β), tumor necrosis factor α (TNF-α), CD4 + and CD8 + levels were detected before and after treatment, the disappearance time of throat irritation, cough cessation time, recovery time of temperature, disappearance time of hoarseness, disappearance time of pharyngeal mucosal congestion, disappearance time of throat foreign body sensation, disappearance time of posterior pharyngeal lymphatic follicular swelling of the two groups were recorded, the traditional Chinese medicine ( TCM) syndrome scores and Functional Swallowing Disorder Screening Scale (EAT10) scores of patients were evaluated, the clinical efficacy and incidences of adverse drug reactions were compared between two groups. RESULTS: The total effective rate of Baihe Liyan capsules group was 95. 20% (119 / 125), higher than 82. 93% ( 102 / 123) of the control group, with statistically significant differences ( P < 0. 05). The recovery time of temperature, disappearance times of throat foreign body sensation, throat irritation, cough, hoarseness, pharyngeal mucosal congestion and posterior pharyngeal lymphatic follicular swelling of the Baihe Liyan capsules group were shorter than those of the control group, with statistically significant differences (P<0. 05). The scores of severe sore throat or pain to ear, dysphagia, pharyngoxerosis, thirst and excessive drinking, constipated, mucousy phlegm, cough, fever, headache and deep-colored urine of the Baihe Liyan capsules group were lower than those of the control group, the EAT10 score of the Baihe Liyan capsules group was significantly lower than that of the control group, with statistically significant differences (P< 0. 05). After treatment, the CD4 + and SIgA levels were higher, the CD8 + level was lowe, the VCAM-1, hs-CRP, IL-1β and TNF-α levels were lower in the Baihe Liyan capsules group than those int he control group, with statistically significant differences (P<0. 05). No obvious adverse drug reactions occurred in either group during treatment. CONCLUSIONS: Baihe Liyan capsules for the treatment of patients with acute laryngopharyngitis of lung-stomach excess-heat syndrome can improve body immunity, reduce inflammatory reaction, enhance throat analgesic effect, promote patients’ recovery, improve the swallowing function and clinical efficacy, with high safety. [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.)

The parasite-mediated sexual selection hypothesis predicts that color expression in color patches of animals can honestly reflect male quality in terms of resistance to parasites. Sceloporine lizards have structural-based blue color patches that can act as intraspecific signals and may thus reflect immunocompetence. However, both color patch expression and intensity of parasitic infections in lizards can vary across seasons. In consequence, we might expect that coloration would honestly reflect immunocompetence to resist parasites only during the mating season. We sampled males of Sceloporus torquatus in central Mexico in spring, summer, and autumn and quantified the reflectance of two structural-based color patches (throat and venter), abundance of two categories of parasites (mites and hemoparasites), and lizards' local inflammatory response to a mitogen (IRM) as a measure of immunocompetence. We examined whether (i) the coloration of lizards changed across seasons in the population, (ii) there is a relationship between coloration and parasite load and/or IRM, and (iii) the latter relationships remained consistent across seasons. Our study shows that color expression seasonally varied; the structural-based coloration of the two patches was significantly more intense in summer, before the mating season. Furthermore, the throat color was more intense in those males with lower parasite load and higher IRM. However, season had no effect on these relationships, suggesting that color expression in the males of S. torquatus can consistently reflect some components of their immunocompetence throughout the year, supporting the honesty of the structural-based coloration in this species. Significance statement: In this study, we aimed to investigate the seasonal variation in structural coloration of a lizard species and its potential relationship with male quality in Torquate lizards (Sceloporus torquatus). Our results revealed distinct seasonal differences in color expression, and furthermore, we found that males displaying more intense blue coloration exhibited lower parasite loads and stronger immune responses. These findings contribute to our understanding of two key aspects: (i) the potential role of structural coloration as an honest signal in organisms of this nature, and (ii) the significance of considering sampling times in organisms with structural coloration, as it can vary throughout the year. [ABSTRACT FROM AUTHOR]

Introduction: The intricate connection between gut microbiota and rheumatoid arthritis (RA) pathogenesis has gained prominence, although the specific microbial species contributing to RA development remain largely unknown. Recent studies have sought to comprehensively explore alterations in the human microbiome, focusing on identifying disease-related microbial species through blood analysis. Consequently, this study aimed to identify RA-associated microbial species using a serum microbial array system and to investigate the efficacy and underlying mechanisms of potential microbial species for RA treatment. Methods: Serum immunoglobulin M levels against 384 intestinal microbial species were assessed using a microbial microarray in patients with RA and healthy individuals. We investigated the therapeutic potential of the identified microbial candidate regarding arthritis development, immune responses, gut barrier function, and gut microbiome using a collagen-induced arthritis (CIA) mouse model. Results: Our findings revealed significant alterations in antibody levels against 36 microbial species in patients with RA compared to healthy individuals. Notably, the antibody levels against Peptoniphilus gorbachii (PG) were decreased in patients with RA and exhibited an inverse correlation with RA disease activity. In vitro experiments demonstrated that PG produced acetate and butyrate, while exhibiting anti-inflammatory properties. In CIA mice, PG administration suppressed arthritis symptoms, reduced the accumulation of inflammatory monocytes in the mesenteric lymph nodes, and downregulated gene expression of pro-inflammatory cytokines in the ileum. Additionally, PG supplementation restored intestinal barrier integrity and partially resolved gut microbial dysbiosis in CIA mice. The fecal microbiota in PG-treated mice corresponded to improved intestinal barrier integrity and reduced inflammatory responses. Conclusion: This study highlights the potential of serum-based detection of anti-microbial antibodies to identify microbial targets at the species level for RA treatment. Moreover, our findings suggest that PG, identified through the microbial microarray analysis, holds therapeutic potential for RA by restoring intestinal barrier integrity and suppressing the immunologic response associated with RA. [ABSTRACT FROM AUTHOR]

Inflammatory skin diseases are a group of diseases caused by the disruption of skin tissue due to immune system disorders. Histone modification plays a pivotal role in the pathogenesis and treatment of chronic inflammatory skin diseases, encompassing a wide range of conditions, including psoriasis, atopic dermatitis, lupus, systemic sclerosis, contact dermatitis, lichen planus, and alopecia areata. Analyzing histone modification as a significant epigenetic regulatory approach holds great promise for advancing our understanding and managing these complex disorders. Additionally, therapeutic interventions targeting histone modifications have emerged as promising strategies for effectively managing inflammatory skin disorders. This comprehensive review provides an overview of the diverse types of histone modification. We discuss the intricate association between histone modification and prevalent chronic inflammatory skin diseases. We also review current and potential therapeutic approaches that revolve around modulating histone modifications. Finally, we investigated the prospects of research on histone modifications in the context of chronic inflammatory skin diseases, paving the way for innovative therapeutic interventions and improved patient outcomes. [ABSTRACT FROM AUTHOR]

Endothelial and epithelial barrier dysfunction due to increased permeability and heightened inflammatory reactions influences the emergence of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). Nevertheless, bibliometric research comparing endothelial and epithelial barriers is limited. Therefore, this bibliometric study analyzed the Web of Science Core Collection (WoSCC) of the Science Citation Index Expanded literature to explore present research priorities and development tendencies within this field. We conducted a comprehensive search (October 18, 2023) on WoSCC from January 1, 2010, to October 18, 2023, focusing on articles related to endothelial and epithelial barriers in ALI and ARDS. Retrieved data were visualized and analyzed using R-bibliometrix, VOS viewer 1.6.19, and CiteSpace 6.2. R4. Functional enrichment analysis of gene targets identified in the keyword list using Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene ontology databases, and based on the STRING database to construct a PPI network to predict core genes. A total of 941 original articles and reviews were identified. The United States had the highest number of publications and citations and the highest H-index and G-index. According to the Collaboration Network Analysis graph, the United States and China had the strongest collaboration. Birukova AA had the most publications and citations among all authors, while eight of the top ten institutions with mediator centrality were located in the United States. The American Journal of Physiology-Lung Cellular and Molecular Physiology was the leading journal and had the most well-established publication on endothelial and epithelial barriers in ALI and ARDS. Bibliometric analysis revealed that the most frequently used keywords were acute lung injury, ARDS, activation, expression, and inflammation. RHOA appeared most frequently among gene-related keywords, and the PI3K-AKT signaling pathway had the highest count in KEGG pathway enrichment. Research on endothelial versus epithelial barriers in ALI and ARDS remains preliminary. This bibliometric study examined cooperative network connections among countries, authors, journals, and network associations in the cited references. Investigation of the functions of the endothelial and epithelial barriers in ALI/ARDS associated with COVID-19 has recently gained significant attention.

Objective: To study the improving effect of Eupatilin (Eptl) on ethanol withdrawal (EtOHWI)-induced anxiety-like behavior in rats and probe the mechanisms related to ventral hippocampus (vHippo). Methods: Thirty-two adult male Sprague-Dawley rats were randomly divided into four groups, 8 rats per group: Saline-treated control group, EtOHWI model group, low-dose Eptl treatment group and high-dose Eptl treatment group. The EtOHWI was established by intraperitoneal injection of 3 g/kg of ethanol (20% volume/volume, dissolved in saline) once a day for 28 days followed by 3 days of withdrawal, during the withdrawal period, the low-and the high-dose Eptl treatment groups were respectively given 10 and 30 mg/kg Eptl through oral route once a day, while the saline control group was administered with an equal volume of saline. Thirty minutes after the third Eptl, all the rats were subjected to open filed (OF) and elevated plus maze (EPM) tests to detect anxiety-like behaviors. The serum coritosterone (CORT) concentration and vHippo γ-aminobutyric acid (GABA) secretion were measured by enzyme linked immunosorbent assay (ELISA), and vHippo glutamic acid decarboxylase 67 (GAD 67) mRNA relative expression was assayed by real-time quantitative polymerase chain reaction. The protein expression of GABAa receptor α1 (GABAaRα1), GABAaRα2, nuclear factor E2-related factor 2 (Nrf2), heme oxygense-1 (HO-1) in the vHippo were analyzed by Western blot. The levels of MDA, T-SOD, CAT and GSH, IL-6 and TNF-α were measured by commercial kits. Meanwhile, in the in vitro experiment, the nuclear levels of Nrf2 in HT22 cells were detected via immunofluorescent technique. Results: Compared with the rats in the EtOHWI group, the rats in low and high-dose Eptl treatment groups moving distance increased significantly (P

The study was to investigate the modulatory effect of Sophora subprosrate polysaccharide (SSP) on inflammatory reaction and immunosuppression in PCV2-infected RAW264.7 cells. The PCV2-infected RAW264.7 cells were treated with SSP (100, 200 and 400 mg/L) for 16 h, the mRNA expression of signal transducer and activator of transcription 1, 2 ( STAT1, STAT2), janus kinase 1 (JAK1), tyrosine kinase 2 (TYK2), chemokine (C-C motif) ligand 3 (Ccl3), chemokine (C-X-C motif) ligand 2 (CXCL2), tumor necrosis factor alpha ( TNF-α), REL proto-oncogene, NF-κB subunit (Rel), nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor alpha and delta (Nfκbia, Nfκbid), and nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor zeta (Nfκbiz) were measured. The protein expression levels of phospho-signal transducer and activator of transcription 1 and 2 (p-Stat1, p-Stat2), signal transducer and activator of transcription 1 and 2 (Stat1, Stat2), inhibitor of nuclear factor κB kinase subunit beta (IκB), phospho-inhibitor of nuclear factor κB kinase subunit beta (p-Iκ B), nuclear factor NF-κB p65 subunit (p65), phospho-nuclear factor NF-κB p65 subunit (p-p65), CXCL2, JAK1, phospho-Janus kinase 1 (p-JAK1) and TYK2 in the cells were detected. The levels of interleukin-1β (IL-1β), interferon-α (IFN-α), interferon-β (IFN-β), and TNF-α in cell supernatants were detected. The results showed that after the RAW264.7 cells were infected with PCV2 for 16 h, the mRNA expression levels of STAT1, STAT2, JAK1, TYK2 and Nfκbia were significantly upregulated (P<0.05), mRNA expression levels of Ccl3, CXCL2, TNF-α, Rel, Nfκbid and Nfκbiz were significantly downregulated ( P<0.05), the protein expression levels of Stat1, p-Stat1, Stat2, p-Stat2, JAK1, p-JAK1 and TYK2 were significantly upregulated ( P<0.05), protein expression levels of IκB, p-IκB, p65 and CXCL2 were significantly downregulated in RAW264.7 cells ( P<0.05), and SSP at 200 mg/L significantly regulated the imbalance in the expression levels of these factors (P<0.05). The study indicates that SSP modulates inflammatory response and immunosuppression induced by PCV2 infection through JAK-STAT/NF-κB signaling pathway. [ABSTRACT FROM AUTHOR]

It is a common experience, reported by patients who have undergone manual therapy that uses deep friction, to perceive soreness in treatment areas; however, it is still not clear what causes it and if it is therapeutically useful or a simple side effect. The purpose of this narrative review is to determine whether manual and physical therapies can catalyze an inflammatory process driven by HA fragments. The literature supports the hypothesis that mechanical stress can depolymerize into small pieces at low molecular weight and have a high inflammatory capacity. Many of these pieces are then further degraded into small oligosaccharides. Recently, it has been demonstrated that oligosaccharides are able to stop this inflammatory process. These data support the hypothesis that manual therapy that uses deep friction could metabolize self-aggregated HA chains responsible for increasing loose connective tissue viscosity, catalyzing a local HA fragment cascade that will generate soreness but, at the same time, facilitate the reconstitution of the physiological loose connective tissue properties. This information can help to explain the meaning of the inflammatory process as well as the requirement for it for the long-lasting resolution of these alterations. [ABSTRACT FROM AUTHOR]

Intracerebral hemorrhage is a common neurological disease, and its pathological mechanism is complex. As the first recruited leukocyte subtype after intracerebral hemorrhage, neutrophils play an important role in tissue damage. In the past, it was considered that neutrophils performed their functions through phagocytosis, chemotaxis, and degranulation. In recent years, studies have found that neutrophils also have the function of secreting extracellular traps. Extracellular traps are fibrous structure composed of chromatin and granular proteins, which plays an important role in innate immunity. Studies have shown a large number of neutrophil extracellular traps in hematoma samples, plasma samples, and drainage samples after intracerebral hemorrhage. In this paper, we summarized the related mechanisms of neutrophil external traps and injury after intracerebral hemorrhage. Neutrophil extracellular traps are involved in the process of brain injury after intracerebral hemorrhage. The application of related inhibitors to inhibit the formation of neutrophil external traps or promote their dissolution can effectively alleviate the pathological damage caused by intracerebral hemorrhage. [ABSTRACT FROM AUTHOR]

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Copyright of China Tropical Medicine is the property of China Tropical Medicine 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.)

Ischemic stroke (IS) is one of the leading causes of death and morbidity worldwide. As a novel form of cell death, ferroptosis is an important mechanism of ischemic stroke. Nuclear factor E2-related factor 2 (Nrf2) is the primary regulator of cellular antioxidant response. In addition to alleviating ischemic stroke nerve damage by reducing oxidative stress, Nrf2 regulates genes associated with ferroptosis, suggesting that Nrf2 may inhibit ferroptosis after ischemic stroke. However, the specific pathway of Nrf2 on ferroptosis in the field of ischemic stroke remains unclear. Therefore, this paper provides a concise overview of the mechanisms underlying ferroptosis, with a particular focus on the regulatory role of Nrf2. The discussion highlights the potential connections between Nrf2 and the mitigation of oxidative stress, regulation of iron metabolism, modulation of the interplay between ferroptosis and inflammation, as well as apoptosis. This paper focuses on the specific pathway of Nrf2 regulation of ferroptosis after ischemic stroke, providing scientific research ideas for further research on the treatment of ischemic stroke. [ABSTRACT FROM AUTHOR]