Tea polysaccharide ameliorates glucolipotoxicity-induced oxidative damage and apoptosis of RIN-m5F cells through Nrf2/HO-1 pathway.

Abstract

Glucolipotoxicity (GLTy) could cause the islet β cell dysfunction in metabolic diseases such as diabetes. Tea polysaccharide (TPS) has the potential to ameliorate islet damage, but its protective effects on GLTY-induced islet β cell damages and its mechanism remain unclear. The RIN-m5F cell damage model was constructed by GLTy induction. The effects of TPS on cell damage were investigated from apoptosis, oxidative stress, inflammatory response, cell senescence and cell function. MTT, ELISA, immunofluorescence, flow cytometry, WB and kits were used to detect cell viability, insulin secretion level, inflammatory factors, antioxidant enzyme activity, cell apoptosis rate and related protein expression. Si-Nrf2 was used to verify whether TPS can activate Nrf2/HO-1 signaling to play a protective role. TPS can increase the cell viability, the positive rate of EdU, insulin secretion, anti-inflammatory factor level, and the activities of SOD and CAT, reduce apoptosis, proinflammatory factor levels and the expression of p21, p53 and p16 proteins. By activating Nrf2/HO-1 pathway, TPS alleviated oxidative stress damage, thus playing a protective role against GLTY-induced cell damage. TPS effectively reduced GLTY-induced RIN-m5F cells damage through activating Nrf2/HO-1 pathway, providing a new idea and potential drug selection for the treatment of diabetes.