Ginsenoside Rh1 Alleviates HK-2 Apoptosis by Inhibiting ROS and the JNK/p53 Pathways

Abstract

Background. Cisplatin is widely used in the treatment of malignant patients; however, its adverse nephrotoxic effects limit its clinical use. Ginsenoside Rh1 is a main component of ginseng and has many pharmaceutical effects, including immunomodulatory effects. Objective. The objective of this research is to assess the effects of ginsenoside Rh1 on a cisplatin-induced HK-2 injury model and to study its potential effect mechanisms. Methods. HK-2 cell vitality was assessed via Cell Counting Kit-8 (CCK-8) assay. Carboxyfluorescein succinimidyl ester/propidium iodide (CFSF/PI) staining was used to detect the apoptosis of HK-2 cells. ROS expression was detected by DCFDA. The expressions of JNK, p53, caspase-3, Bax, and NGAL were detected by western blot. Results. Ginsenoside Rh1 was found to increase the vitality of HK-2 cells and inhibit ROS production and the apoptosis of HK-2 cells in a cisplatin-induced injury model. Ginsenoside Rh1 was found to inhibit the expression of JNK, p53, caspase-3, Bax, and NGAL in a cisplatin-induced injury model. Conclusion. Ginsenoside Rh1 alleviated HK-2 apoptosis in a cisplatin-induced injury model by inhibiting ROS production and the JNK/p53 pathway. Ginsenoside Rh1 may be a promising drug for the alleviation of cisplatin-induced nephrotoxicity in malignant patients.