Astilbin inhibits high glucose-induced autophagy and apoptosis through the PI3K/Akt pathway in human proximal tubular epithelial cells

Diabetic nephropathy (DN) is the leading cause of end-stage renal disease. It has been found that astilbin, a flavonoid compound, exerts a protective effect on DN. However, the role of astilbin in autophagy during DN is unknown. The human proximal tubular epithelial cells (HK-2 cells) were treated with high glucose (HG, 30 mM) in the presence or absence of astilbin. Cell viability was measured by MTT assay. The autophagy was determined by detecting the expression of LC3-II and p62 using western blot. The cell apoptosis was evaluated by detecting the apoptosis rate, caspase-3 activity, and the expression of Bcl-2 and Bax. The expression levels of protein kinase B (Akt) and p-Akt were detected by western blot. To determine whether the phosphatidylinosito1-3-kinase (PI3K)/Akt pathway was involved in the effect of astilbin, cells were treated with the inhibitor of Akt, LY294002. We found that astilbin (10 and 20 mu M) did not affect the viability of HK-2 cells, but attenuated HG-induced cell viability. Astilbin attenuated HG-induced autophagy and apoptosis in HK-2 cells. The expression of p-Akt was inhibited by HG treatment, while the inhibitory effect of HG was attenuated by astilbin. Inhibition of the PI3K/Akt signaling resisted the effect of astilbin on HG-induced apoptosis and autophagy. In conclusion, astilbin attenuated HG-induced autophagy and apoptosis in HK-2 cells through the PI3K/Akt pathway. The results indicated that astilbin might be a new therapeutic agent and be useful for improving clinical management of DN.