Protective Effect Of Pseudoginsenoside F11on Cisplatin Induced Nephrotoxicity And Its Molecular Mechanism

Objective Renal injury model was estabLished with cispLatin (CDDP) to research theprotective effect of Pseudoginsenoside F11and to explore its possible molecular protectionmechanisms; anti-tumor effect was explored by Pseudoginsenoside F11combination withcisplatin.Methods MTT assay was used to explore the cytotoxicity of Pseudoginsenoside F11combination with cisplatin; a single injection of cisplatin (6mg/kg, i.p)was used toestablish rat kidney injury model to explore the protect function and molecularmechanisms of injury renal.C57BL/6J mice bearing Lewis lung cancer and B16melanomamodle was established to observe the anti-tumor effects of Pseudoginsenoside F11combination whith cisplatin.Results In vitro experiments showed that co-administration of Pseudoginsenoside F11andcisplatincan significantly increase the survivalof rat renal podocytes (#P <0.05,*P <0.01).In vivo, cispLatin (6mg/kg, i.p) enables serum BUN and Cr increased significantly(*P <0.01), serum markers significantly decreaced, the rat renal tissue oxygenation indexand apoptosis-related protein expression were significantly restored after oraladministration of Pseudoginsenoside F11.Tumor-bearing mice experiments showedPseudoginsenoside F11after plus cisplatin administration does not affect the play ofcisplatin,s anti-cancer effect.Conclusion Pseudoginsenoside F11can reduce cisplatin-induced renal injury inrats,which may be improved by the endogenous antioxidant capacity, particuLarly to prevent the DNA breakage of renal proximl tubule cell, reduce the leakage of P53proteinin the cytoplasm outside the nucleus, thereby reducing the effects of cisplatin onmitochondrial morphology and function, reducing the intracellular expression of Caspasefamily, and ultimately prevent apoptosis of renal cells. Meanwhile, Pseudoginsenoside F11administration plus cisplatin did not affect its anti-cancer effect.