Esculentoside A exerts anti-oxidative stress and anti-apoptotic effects in rat experimental membranous nephropathy by regulating MAPK pathway

Background Membranous nephropathy is characterized by deposition of immune complex. The initial inflammatory responses induce cell apoptosis and oxidative injury, thus contributing to the pathogenesis of chronic kidney disease. Esculentoside A exerts anti-inflammatory, anti-apoptotic and anti-oxidant abilities, and protects against acute kidney injury. Objective The renoprotective effect of Esculentoside A on a rat model with membranous nephropathy was investigated in this study. Results Injection of cationic bovine serum albumin promoted the level of 24 h proteinuria, and induced histopathological damage, including glomerular atrophy and thick glomerular basement membrane in the kidney tissues. Intraperitoneal injection with Esculentoside A reduced the level of 24 h proteinuria, and attenuated the pathological damages. Esculentoside A attenuated cationic bovine serum albumin-induced reduction of Bcl-2 protein expression, enhancements in the protein expressions of Bax and cleaved caspase-3. Besides, the enhanced levels of MDA (malondialdehyde) and NO (nitric oxide), and reduced levels of SOD (superoxide dismutase) and GSH (glutathione), in rats with membranous nephropathy were restored by Esculentoside A injection. Moreover, Esculentoside A counteracted with the promotive effects of cationic bovine serum albumin on the protein expressions of phosphorylated JNK (p-JNK), p-ERK1/2 and p-p38. Conclusion The renoprotective effects of Esculentoside A on a rat model with membranous nephropathy was mediated by its anti-oxidant and anti-apoptotic effects through inactivation of MAPKs pathway.