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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 observe the effect of edaravone on gentamicin-induced renal tubular epithelial cell injury and its mechanism. Methods: Rat renal tubular epithelial cells (NRK-52E) were subcultured and divided into control group, injury group (2mg / ml gentamycin), treatment group A (2mg / ml gentamycin + 10μmol / (2mg / ml gentamicin + 20μmol / ml edaravone) and C (2mg / ml gentamycin + 40μmol / ml edaravone) were used to observe the cell proliferation, lactate Dehydrogenase (LDH) level, malondialdehyde (MDA) content, superoxide dismutase (SOD) activity, apoptosis rate and the expression of bcl-2 and Bax mRNA. RESULTS: After gentamicin stimulated NRK-52E cells, the cell proliferation decreased, the content of LDH and MDA increased, the activity of SOD decreased, the apoptosis increased and the expressions of bcl-2 and Bax mRNA increased. Edaravone can increase cell proliferation, decrease LDH and MDA, increase SOD activity, decrease apoptosis, up-regulate bcl-2 mRNA and down-regulate Bax mRNA expression. These changes are obvious with dose increasing (all P <0.05). Conclusion: Edaravone can reduce gentamicin-induced tubular epithelial cell injury in rats. The mechanism may be related to reducing oxidative stress and inhibiting apoptosis.