Gastrodin inhibits high glucose-induced inflammation, oxidative stress and apoptosis in podocytes by activating the AMPK/Nrf2 signaling pathway

Diabetic nephropathy (DN) is a serious and common complication of type 1 and 2 diabetes. Gastrodin has been reported to suppress high glucose (HG)-induced inflammation and oxidative stress in vivo and in vitro. However, the effect of gastrodin on DN has not been fully elucidated. The present study aimed to investigate the underlying mechanism involved in the effect of gastrodin on podocyte injury caused by DN. Cell viability was evaluated using Cell Counting Kit-8 assay and secretion levels of TNF-alpha, IL-1 beta and IL-6 were measured using ELISA. The levels of malondialdehyde, activities of lactate dehydrogenase and superoxide dismutase were quantified using corresponding assay kits. Additionally, cell apoptosis was analyzed by TUNEL assay, whilst protein expressions related to inflammation, apoptosis and the 5'-AMP-activated protein kinase (AMPK)/nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway were measured by western blot analysis. The results showed that gastrodin increased the viability of MPC5 cells following HG stimulation. Gastrodin also alleviated HG-induced inflammation, oxidative stress and apoptosis in MPC5 cells. Furthermore, gastrodin promoted activation of the AMPK/Nrf2 pathway in MPC5 cells. Treatment with the AMPK inhibitor, compound C, reversed the inhibitory effects of gastrodin on inflammation, oxidative stress and cell apoptosis. To conclude, treatment of MPC5 cells with gastrodin can attenuate HG-induced inflammation, oxidative stress and cell apoptosis by activating the AMPK/Nrf2 signaling pathway. Results from the current study suggest that gastrodin can be used as an effective therapeutic agent against HG-induced podocyte injury in DN.