Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Rehmannioside A protects against high glucose-induced apoptosis and oxidative stress of renal tubular epithelial cells by inhibiting the MAPK pathway

Lili Yang¹, Lei Huai² , Qunhong Xu¹, Benyong Wang¹

¹Department of Nephrology; ²Department of Central Laboratory, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310006, China.

For correspondence:- Lei Huai Email: huailei_666@163.com Tel:+8657156007165

Accepted: 30 July 2021 Published: 31 August 2021

Citation: Yang L, Huai L, Xu Q, Wang B. Rehmannioside A protects against high glucose-induced apoptosis and oxidative stress of renal tubular epithelial cells by inhibiting the MAPK pathway. Trop J Pharm Res 2021; 20(8):1553-1558 doi: 10.4314/tjpr.v20i8.1

© 2021 The authors.
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Abstract

Purpose: To investigate the effects and mechanism of rehmannioside A (ReA) on diabetic nephropathy (DN) progression.

Methods: Various concentrations of glucose and ReA were added to HK2 cells, and cell viability was analyzed using the 3-(4,5)-dimethylthiahiazo(-2)-3,5-diphenytetrazoliumromide (MTT) assay. Cell apoptosis, caspase 3 activity, and expression levels of BAX, Bcl-2, and cleaved poly (ADP-ribose) polymerase were evaluated to assess the effect of ReA on cell apoptosis. The effect of ReA on oxidative stress was also evaluated by assessing superoxide dismutase, catalase, and malondialdehyde levels. Lactate dehydrogenase release and reactive oxygen species levels were also measured. Finally, activation of p38 mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinase 1/2 was determined by immunoblot technique.

Results: ReA significantly enhanced the survival of HK2 cells induced with high glucose (HG). In addition, ReA suppressed apoptosis and inhibited oxidative stress of HK2 cells induced with HG (p < 0.05). ReA protected against HG-induced apoptosis and oxidative stress of renal tubular epithelial cells by inhibiting the MAPK pathway (p < 0.05).

Conclusion: ReA is a potential as a therapeutic agent for DN; however, in vivo and clinical investigations are required to validate this assertion.

Keywords: Diabetic nephropathy, Rehmannioside, Apoptosis, Oxidative stress, MAPK pathway, HK2 cells