依达拉奉对庆大霉素诱导肾小管上皮细胞损伤的保护作用

Protective Effect of Edaravone Against Rat Renal Tubular Epithelial Cell Damage Induced by Gentamicin

目的:观察依达拉奉对庆大霉素诱导大鼠肾小管上皮细胞损伤的作用及其机制。方法:传代培养大鼠肾小管上皮细胞(NRK-52E),分为对照组、损伤组(2mg/ml庆大霉素)、治疗组A(2mg/ml庆大霉素+10μmol/ml依达拉奉)、B(2mg/ml庆大霉素+20μmol/ml依达拉奉)和C(2mg/ml庆大霉素+40μmol/ml依达拉奉),观察各组细胞增殖能力、乳酸脱氢酶(LDH)水平、丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性、细胞凋亡率以及bcl-2和Bax mRNA表达情况。结果:庆大霉素刺激NRK-52E细胞后,细胞增殖能力下降、LDH和MDA含量升高、SOD活性下降、细胞凋亡增加、bcl-2和Bax mRNA表达增多。依达拉奉可以提高细胞增殖能力、降低LDH和MDA含量、增强SOD活性、减少细胞凋亡、上调bcl-2mRNA表达以及下调Bax mRNA表达;这些改变随剂量增加而明显(P均<0.05)。结论:依达拉奉可以减轻庆大霉素诱导的大鼠肾小管上皮细胞损伤,其机制可能与减轻氧化应激、抑制细胞凋亡有关。

Objective：To investigate the protective effect and its mechanism of edaravone against rat renal tubular eepithelial cell damage induced by gentamicin.Methods：The rat renal tubular epithelial cells（NRK-52E）were divided into control group,damage group（2mg/ml gentamicin）,treatment group A（2mg/ml gentamicin plus 10μmol/ml edaravone）,B（2mg/ml gentamicin plus 20μmol/ml edaravone）and C（2mg/ml gentamicin plus 40μmol/ml edaravone）.The cell proliferation ability,concentrations of lactate dehydrogenase（LDH）in cell culture supernatant,content of malondialdehyde,activity of superoxide dismutase（SOD）,rate of apoptosis,express of bcl-2mRNA and Bax mRNA of cell were detected.Results：In damage group,proliferation ability and activity of SOD of cell were decreased,concentrations of LDH in cell culture supernatant,content of malondialdehyde,rate of apoptosis,express of bcl-2mRNA and Bax mRNA of cell were in-creased as compared with control group.Compared to damage group,proliferation ability,activity of SOD and express of bcl-2mRNA of cell were increased and concentrations of LDH in cell culture supernatant,content of malondialdehyde,rate of apoptosis,express of Bax mRNA of cell were decreased in treatment group,with all of those change were dose-dependent of edaravone from 10μmol/ml to 40μmol/ml.Conclusion：Edaravone can alleviate rat renal tubular epithelial cell damage induced by gentamicin,via inhibiting oxidative stress and down-regulating cell apoptosis.