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Ginsenoside Rg1 attenuates arsenic-induced mice nephrotoxicity via the activated HO-1/mTOR-associated apoptosis or autophagy signaling

Nephrotoxicity attributed to environmental arsenic exposure, has been recognized by animal experiments and populational survey over 30 years in China, given a significance of public health by preventing from the disorder of renal function and hispathological abnormality.
 Here, Ginsenoside Rg1 (Rg1) as the commercial bioactive product of ginseng, play a beneficial role via antioxidant, anti-inflammatory and anti-apoptotic effects, which is poorly understood in arsenic-induced nephrotoxicity. The present study applied animal experiments to explore the pharmacological effects of Rg1 on sodium arsenite (SA)-induced nephrotoxicity in mice. Results showed that SA exposure led to renal pathological damage, and induced renal oxidative stress and the elevated levels of apoptosis or autophagy-associated indices in kidney. Further, western-blotting results confirmed the upregulations of pro-apoptotic Bax or autophagic unc-51-like kinase-1 (ULK1) or LC3-B signal, and the downregulations of HO-1 or mTOR signal and autophagy substrate sequestosome 1 (p62/SQSTM1) in kidney. Significantly, the intervention with Rg1 alleviated arsenic-induced renal pathological damage and oxidative stress, and upregulated the levels of HO-1, mTOR and p62, while the levels of Bax, ULK1 or LC3-B downregulated in kidney. In conclusion, the intervention with Rg1 relieves arsenic-induced mice nephrotoxicity maybe involved in the regulation of HO-1/mTOR-related apoptotic or autophagic signaling.