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目的:观察阿米卡星对肾小管上皮细胞的损伤及热休克蛋白70表达的影响。方法:常规培养人肾小管上皮细胞系HK-2细胞,给予阿米卡星(100μg·mL-1)损伤或MnCl2(2μg·mL-1)保护,于24,48,72,96 h时分光光度法测定细胞增殖,乳酸脱氢酶(LDH)、超氧化物歧化酶(SOD)、丙二醛(MDA)、N-乙酰-β氨基葡萄糖苷酶(NAG)含量,逆转录多聚酶链式反应(RT-PCR)法检测HSP70 mRNA表达,Western-blot检测HSP70蛋白表达。结果:阿米卡星损伤HK-2细胞后,细胞增殖显著减少,LDH释放量、NAG含量、MDA含量增加显著,SOD活力明显下降,HSP70 mRNA及其蛋白的表达显著增加(与对照组比,P<0.01);给予MnCl2干预后,HK-2细胞的细胞增殖明显有所恢复,LDH释放量、NAG含量、MDA含量有所下降,SOD活力有所增加,HSP70 mRNA及其蛋白的表达有所下降(与损伤组比,P<0.01)。结论:阿米卡星的肾脏毒性与HSP70的表达存在密切的联系。
Objective: To observe the effect of amikacin on renal tubular epithelial cells and the expression of heat shock protein 70 (HSP70). Methods: Human renal tubular epithelial cell line HK-2 cells were cultured routinely. The cells were protected by amikacin (100μg · mL-1) or MnCl2 (2μg · mL-1), and divided into light at 24,48,72,96 h The cell proliferation, the content of lactate dehydrogenase (LDH), superoxide dismutase (SOD), malondialdehyde (MDA), N-acetyl-β-glucosaminidase The expression of HSP70 mRNA was detected by RT-PCR and the expression of HSP70 was detected by Western-blot. Results: The proliferation of HK-2 cells was significantly reduced after amikacin injury. The release of LDH, NAG and MDA were significantly increased, the activity of SOD was significantly decreased and the expression of HSP70 mRNA and protein were significantly increased (compared with the control group, P <0.01). After the intervention of MnCl2, the cell proliferation of HK-2 cells was obviously recovered, the release of LDH, the content of NAG and the content of MDA decreased, the activity of SOD increased and the expression of HSP70 mRNA and protein Decreased (compared with the injury group, P <0.01). Conclusion: There is a close relationship between the toxicity of amikacin and the expression of HSP70.