参百益通过诱导自噬和抑制NLRP3炎症小体保护顺铂诱导的HK-2细胞损伤

Shenbaiyi protects HK-2 cells injury induced by cisplatin by activating autophagy and inhibiting NLRP3 inflammasome

目的:考察参百益的有效成分人参皂苷Rg3对顺铂诱导人肾小管上皮细胞(HK-2)损伤的保护作用和作用机制。方法:利用MTT法检测参百益和顺铂对HK-2细胞存活率的影响,通过Western blot法和荧光免疫检测法对HK-2细胞内炎症和自噬相关蛋白的表达进行检测。结果:参百益抑制了顺铂诱导的HK-2细胞凋亡,使HK-2细胞的存活率显著升高。参百益与顺铂联合作用,使NLRP3、p-p65和p62的表达显著降低,LC3II/I和Becline-1的表达明显升高。结论:参百益与顺铂联用,可以通过抑制炎症小体激活和诱导细胞自噬,减弱顺铂的肾毒性,为参百益的临床应用提供了理论依据。

OBJECTIVE To investigate the protective effect and mechanism of ginsenoside Rg3,the active ingredient of Shenbaiyi,on human renal tubular epithelial cells(HK-2)injury induced by cisplatin.METHODS The effect of Shenbaiyi and cisplatin on the survival rates of HK-2 cells were detected by MTT assay,and the expressions of proteins in HK-2 cells were detected by Western blot and fluorescence immunoassay.RESULTS Shenbaiyi inhibited the apoptosis of HK-2 cells induced by cisplatin,and significantly increased the survival rates of HK-2 cells.The combination of Shenbaiyi and cisplatin significantly reduced the expression of NLRP3,p-p65 and p62 proteins,while increasing the expression of LC3 II/I and Becline-1 proteins.CONCLUSION Shenbaiyi combined with cisplatin can reduce the renal toxicity of cisplatin by inhibiting the expression of NLRP3 inflammasome and activating autophapy,providing a theoretical basis for the clinical application of Shenbaiyi.