Alisol B 23-Acetate Affects a Podocyte Injury Model by Inhibiting PI3K/AKT/mTOR Signaling

Diabetic nephropathy is the leading cause of impaired renal function. Podocyte injury is a crucial factor during the pathological process of diabetic nephropathy. This study aimed to explore the function and mechanism of alisol B 23-acetate in modulating podocyte injury. Podocytes exposed to a high concentration of glucose were used to establish an in vitro cell model. The concentration of proinflammatory factors was evaluated by enzyme-linked immunosorbent assay. Podocyte viability and apoptosis were examined by cell counting kit 8 assays and flow cytometry. The levels of malondialdehyde and the activities of superoxide dismutase and catalase in podocytes were assessed using corresponding assay kits. Western blot analysis was performed to measure the protein levels of apoptosis-related markers, inflammation-related markers, and indicators of oxidative stress. The results revealed that high glucose induced podocyte injury by suppressing viability and accelerating apoptosis in podocytes, and this effect was reversed by alisol B 23-acetate. Additionally, alisol B 23-acetate prevented high glucose-induced oxidative stress and inflammation in podocytes. The activation of PI3K/Akt/mTOR signaling induced by high glucose was inhibited by alisol B 23-acetate in podocytes. After the PI3K/Akt/mTOR pathway was inactivated using BEZ235 (a dual PI3K and mTOR inhibitor), the suppressive effects of alisol B 23-acetate on high glucose-induced apoptosis, oxidative stress and inflammation in podocytes were enhanced.