Schizandrin B inhibits the cis‑DDP‑induced apoptosis of HK‑2 cells by activating ERK/NF‑κB signaling to regulate the expression of survivin.

The nephrotoxicity of cisplatin limits its clinical application. Schizandrin B (SchB) has been demonstrated to have a variety of potential cytoprotective activities. The present study explored the molecular mechanisms by which SchB inhibits the dichlorodiammine platinum (DDP)‑induced apoptosis of HK‑2 proximal tubule epithelial cells. In vitro assays demonstrated that SchB increased the viability of HK‑2 cells, alleviated the cis‑DDP‑induced activation of caspase‑3, reduced apoptosis and improved the nuclear morphology of HK‑2 cells. Additionally, the mechanism underlying the cis‑DDP‑induced apoptosis was indicated to involve the activation of p53, c‑Jun‑N‑terminal kinase (JNK) and p38 signaling. Furthermore, SchB was demonstrated to activate extracellular signal‑regulated kinase (ERK) and nuclear factor κB (NF‑κB) signaling, and induce the expression of survivin. The inhibition of ERK and NF‑κB signaling using U0126 and pyrollidine dithiocarbamate, respectively, inhibited the expression of survivin, whereas blocking the expression of survivin using small interfering RNA inhibited the alleviating effect of SchB on cis‑DDP‑induced apoptosis as indicated by a reduction in cleaved caspase‑3 expression. In conclusion, SchB regulates ERK/NF‑κB signaling to induce the expression of survivin, thereby alleviating cis‑DDP‑induced renal injury.