Tripterygium glycoside protects against puromycin amino nucleoside‑induced podocyte injury by upregulating autophagy.

Tripterygium glycoside (TG), an active ingredient of the widely used Chinese herb Tripterygium wilfordii Hook F, has immunosuppressive and anti‑inflammatory effects. Previous studies have indicated that TG is a potentially effective therapeutic option to treat nephrotic syndrome. The mechanism underlying the therapeutic effect of TG, including its effect on autophagy and apoptosis in podocyte injury, remains to be fully elucidated. The present study aimed to assess the protective effect of TG on podocytes via its potential role in the activation of autophagic and phosphatidylinositol 3‑kinase (PI3K) pathways. Using flow cytometry, western blot analysis, cell counting kit‑8 assays and transmission electron microscopy analysis, the effects of TG on puromycin aminonucleoside (PAN)‑induced podocyte injury were investigated. Chloroquine (CQ), an inhibitor of autophagy, was used to assess the importance of autophagy in the protective effect of TG. In addition, LY294002, an inhibitor of class III PI3K, was used to identify which signaling pathways TG is involved in. PAN caused marked apoptosis of podocytes, which was significantly antagonized by TG. The expression of microtubule‑associated protein 1A/1B‑light chain 3 and the appearance of autophagosomes increased significantly following TG treatment, whereas the expression levels of p62 and cleaved caspase-3 were markedly decreased. Podocyte apoptosis decreased significantly when the podocytes were treated with TG compared with the levels of apoptosis in the PAN‑ and PAN+CQ‑treated groups. The expression of phosphorylated AKT was increased significantly in the TG‑treated groups, and the effects of TG on the podocytes were significantly inhibited by LY294002. In conclusion, TG protected podocytes from PAN‑induced injury, and the effects were attributable to the activation of autophagy, mainly via a PI3K‑dependent pathway.