Molecular medicine reports
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Osteoarthritis (OA) has a high prevalence in female patients and sex may be a key factor affecting the progression of OA. The aim of the present study was to identify genetic signatures in the synovial membranes of female patients with OA and to elucidate the potential associated molecular mechanisms. The gene expression profiles of the GSE55457 and GSE55584 datasets were obtained from the Gene Expression Omnibus database. ⋯ KEGG pathway analysis indicated that the DEGs included in the top one module were mainly enriched in the 'ribosome' pathway. The present study provides a systematic, molecular‑level understanding of the degeneration of the synovial membrane in the progression of OA in female patients. The hub genes and molecules associated with the synovial membrane may be used as biomarkers and therapeutic targets for the treatment of OA in female patients with OA.
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Inflammation is a defensive response in the living tissue of the vascular system that acts against damage factors and involves various types of immune cells, including macrophages, neutrophils, endothelial cells and other associated immune molecules. If the release of inflammatory mediators is excessive, systemic inflammatory response syndrome may develop. Sepsis is the most common complication of severe burns and is a systemic inflammatory response syndrome that is caused by infectious factors and is capable of leading to multiple organ dysfunction and potentially death. ⋯ The results of the present study demonstrated that BMSCs co‑cultured with macrophages directly inhibited macrophage differentiation into the M1 phenotype and reduced inflammation in macrophages stimulated by LPS. In vivo, BMSCs decreased the expression of CD11c in peritoneal macrophages and reduced the pathological inflammatory response in the lungs. The findings of the present study demonstrated that BMSCs may reduce the extent of the systemic inflammatory response, which may contribute to the development for a novel type of treatment for sepsis in the future.
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Reactive oxygen species (ROS) are implicated in the pathogenesis of thrombosis. Studies have reported that resveratrol exhibits antioxidative activities, however, the effect and underlying mechanisms of resveratrol on venous thrombosis remain largely unknown. To investigate the effect of resveratrol on venous thrombosis and the underlying mechanisms, the present study investigated the effects of resveratrol on cell viability, apoptosis, ROS generation and the expression of thrombosis‑associated markers in human umbilical vein endothelial cells (HUVECs). ⋯ Resveratrol also significantly inhibited the induction of phosphorylated (p)‑p38, P‑c‑Jun N‑terminal kinase and P‑extracellular signal‑regulated kinase by H2O2, and these effects were attenuated by the MAPK pathway activators anisomycin and curcumin. In conclusion, these results indicate that resveratrol protected HUVECs against oxidative stress and apoptosis. Furthermore, to the best of our knowledge, the present study is the first to demonstrate that resveratrol attenuates the expression of thrombosis‑associated markers induced by H2O2, which may occur through the suppression of the MAPK signalling pathways, indicating a potential novel therapeutic approach to prevent venous thrombosis.
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Sepsis is a life-threatening condition in which an uncontrolled inflammatory host response is triggered. The exact pathogenesis of sepsis remains unclear. The aim of the present study was to identify key genes that may aid in the diagnosis and treatment of sepsis. mRNA expression data from blood samples taken from patients with sepsis and healthy individuals was downloaded from the Gene Expression Omnibus database and differentially expressed genes (DEGs) between the two groups were identified. ⋯ Furthermore, RT‑qPCR results demonstrated that IRAK3, adrenomedullin (ADM), arachidonate 5‑lipoxygenase (ALOX5), matrix metallopeptidase 9 (MMP9) and S100A8 were significantly upregulated, while ectonucleoside triphosphate diphosphohydrolase 1 (ENTPD1) was upregulated but not significantly, in blood samples from patients with sepsis compared with healthy individuals, which was consistent with bioinformatics analysis results. Therefore, AGTRAP, IRAK3, ADM, ALOX5, MMP9, S100A8 and ENTPD1 were identified to have potential diagnostic value in sepsis. In conclusion, dysregulated levels of the AGTRAP, IRAK3, ADM, ALOX5, MMP9, S100A8 and ENTPD1 genes may be involved in sepsis pathophysiology and may be utilized as potential diagnostic biomarkers or therapeutic targets.
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The current study aimed to investigate the effects of the thymic stromal lymphopoietin (TSLP)/TSLP receptor (TSLPR) on angiogenesis following ischemic stroke in vivo and in vitro. Furthermore, whether the phosphatidylinositol 3 kinase (PI3K)/protein kinase B (AKT) pathway mediates the effects of TSLP/TSLPR on angiogenesis was explored. A rat middle cerebral artery occlusion (MCAO) model was established, and it was demonstrated that the expression levels of TSLP and TSLPR were significantly increased in the infarct area between 12 and 72 h after MCAO, as determined by ELISA and western blot analyses. ⋯ In conclusion, to the best of our knowledge, this study demonstrated for the first time that TSLP/TSLPR promote angiogenesis following ischemic stroke in vivo and in vitro. Furthermore, it was demonstrated that the effects of TSLP/TSLPR on angiogenesis were, at least partially, mediated via activation of the PI3K/AKT pathway. TSLP/TSLPR may serve as a potential therapeutic target for ischemic stroke treatment.