Resveratrol improves Gly-LDL-induced vascular endothelial cell apoptosis, inflammatory factor secretion and oxidative stress by regulating miR-142-3p and regulating SPRED2-mediated autophagy

Background: Resveratrol improves cell apoptosis and tissue damage induced by high glucose, but the specific mechanism is unknown. Methods: This is a basic research. We performed cell transfection, real-time fluorescence quantitative PCR (qPCR), flow cytometry, immunofluorescence, western blot, enzyme linked immunosorbent assay (ELISA) and cell viability assay to analyze cell viability, cell cycle, cellular oxidative stress, intracellular inflammatory factors and autophagy activities in vitro. Meanwhile, dual luciferase reporter assay was conducted to explore the influence of miR-142-3p and sprouty-related EVH1 domain 2 (SPRED 2) on human glycated low-density lipoprotein (Gly-LDL)-induced vascular endothelial cell apoptosis, inflammatory factor secretion and oxidative stress. Results: Resveratrol inhibited the expression of miR-142-3p in human umbilical vein endothelial cells (HUVECs) induced by Gly-LDL in a dose-dependent manner, and the overexpression of miR-142-3p reverses the effect of resveratrol on the proliferation, apoptosis, secretion of inflammatory factors, oxidative stress, and autophagy. The dual-luciferase report analysis found a negative regulatory relationship between miR-142-3p and SPRED2. Inhibition of SPRED2 reversed the effects of resveratrol on Gly-LDL-induced HUVECs proliferation, apoptosis, inflammatory factor secretion and oxidative stress, and reversed the effects of resveratrol on Gly-LDL-induced HUVECs autophagy. Conclusion: miR-142-3p promotes the development of diabetes by inhibiting SPRED2-mediated autophagy, including inducing cell apoptosis, aggravating cellular oxidative stress and secretion of inflammatory factors, and resveratrol improves this effect.

Automated summary

Resveratrol improves cell apoptosis and tissue damage induced by high glucose by regulating the miR-142-3p and SPRED2-mediated autophagy pathway. The study suggests a promoting role of miR-142-3p and an inhibitory role of SPRED2 in the development of diabetes.