The results demonstrated that high glucose suppressed HLEC viability and proliferation rate compared with normal glucose levels (5 mM), which were significantly reversed by resveratrol treatment. High glucose also increased the ROS content compared with ROS content in normal HLECs, which was reduced following resveratrol treatment. Further experiments demonstrated that resveratrol significantly reversed the high glucose-decreased protein levels of LC3II and beclin-1 proteins and the high glucose-increased protein levels of LC3I and p62 in HLECs. In conclusion, resveratrol inhibited the high glucose-induced oxidative damage in HLECs by promoting autophagy through the activation of the p38 mitogen-activated protein kinase signaling pathway. These results provide a theoretical basis for the application of resveratrol in diabetic cataract prevention and treatment.Peroxiredoxin 3 (PRDX3) is an abundant and effective enzyme, which aids in the removal of H2O2 in the mitochondria, thereby inhibiting cell autophagy. PRDX3 is a target protein of microRNA (miRNA/miR)-383, the overexpression of which has been found to inhibit the growth of glioma cells. We hypothesized that miR-383 serves an antitumor role by inhibiting oxidative stress during tumor growth. In the current study, human glioma U87 cells were transfected with pre-/short hairpin (sh)-PRDX3 vectors and miR-383 mimics/inhibitors. Apoptosis and reactive oxygen species (ROS) production were detected using flow cytometry. Autophagy was examined using acridine orange staining, and the expression of cytoplasmic autophagy-related proteins [autophagy-related protein 9 (ATG9), Ras-related protein Rab-1A (Rab1) and p62] was determined using western blot analysis. The interaction between miR-383 and PRDX3 was assessed using a dual-luciferase assay. The results indicated that both sh-PRDX3 and miR-383 mimics promoted apoptosis and increased the level of mitochondrial ROS, whilst acridine orange staining revealed that sh-PRDX3 promoted autophagy in U87 cells compared with that in the control cells. The detection of autophagic proteins indicated that sh-PRDX3 and miR-383 mimics increased the protein expression level of ATG9 and RAB1, and inhibited that of p62. On the contrary, the effect of miR-383 mimics was opposite to that of pre-PRDX3 in U87 cells. Reverse transcription-quantitative PCR and western blot assays revealed that miR-383 was negatively associated with PRDX3 in U87 cells. miR-383 was indicated to interact with PRDX3, as demonstrated using a dual-luciferase assay. In conclusion, the present study demonstrated that miR-383 induced cell apoptosis and mitochondrial ROS production by downregulating PRDX3 in U87 cells, thereby promoting oxidative stress-induced autophagy.Shear stress has been reported to result in various metabolic effects in endothelial cells (ECs), which in turn contribute to the regulation of their vascular functions. Peroxisome proliferator-activated receptors (PPARs) have been reported to regulate lipid metabolism and have been implicated in metabolic disorders. The present study assessed the effects of laminar shear stress on the expression of PPARs in ECs in the presence of high concentrations of free fatty acids (FFAs). Human aortic ECs (HAECs) were treated with a high concentrations of palmitic acid (PA) and exposed to high shear stress (HSS) or low shear stress (LSS). Western blotting and ELISA were performed to quantify protein expression and assess prostacyclin production. https://www.selleckchem.com/products/cpypp.html The results revealed that long-term application of HSS to PA-treated HAECs induced PPAR-α, -δ and -γ protein expression. Additionally, LSS induced higher levels of PPAR-α protein expression in PA-treated HAECs compared with those after HSS. HAECs exposed to HSS also released prostacyclin (PGI2). However, HAECs treated with high concentrations of PA also produced high levels of PGI2 in the perfusion media in response to HSS compared with the static PA group. HSS also reduced the static PA-induced expression of intercellular adhesion molecule-1 and monocyte chemoattractant protein-1. The results demonstrated that HAECs increases the expression of all three peroxisome proliferator-activated receptor isoforms in response to shear metabolic stress at high FFA concentrations. The present study may provide preliminary insights into the potential roles of PPARs as an effective treatment method against metabolic disturbances that can result in EC dysfunction.Enhancer of zeste homolog 2 (EZH2) is positively associated with poor clinical outcomes in a number of aggressive tumors. Recent studies have demonstrated that inhibition of EZH2 also suppressed the inflammatory response during sepsis. The present study aimed to investigate whether an inhibitor of EZH2, GSK343, could protect the intestine against sepsis-induced injury in vivo. Mice underwent cecal ligation and perforation (CLP) to induce sepsis and were assigned into three groups Sham, CLP and CLP + GSK343. For GSK343 treatment, the septic mice were intravenously injected with GSK343 at 6 h post-CLP. The results indicated that EZH2 was highly expressed while tight junction (TJ) proteins ZO-1, occludin and claudin-1 expression was reduced in the intestinal tissue of mice subjected to CLP compared with the sham group. CLP operation also caused intestinal pathological injury and the production of inflammatory cytokines including TNF-α, IL-1β and IL-6 in both serum and intestinal tissues. Meanwhile, CLP induced cell apoptosis of intestinal tissue based on the increased number of apoptotic cells, reduced expression of Bcl-2 and higher expression of caspase-3 and Bax. However, the presence of GSK343 partially rescued intestinal pathological injury, reduced the level of inflammatory cytokines, repressed cell apoptosis and promoted TJ protein expression. Finally, the decreased number of Paneth cells caused by CLP operation was reversed by GSK343 treatment. In conclusion, the results of the present study demonstrated that GSK343 could protect the intestine against sepsis-induced injury in vivo. Inhibition of EZH2 may provide a therapeutic approach for intestinal dysfunction during sepsis.