缺氧-复氧后HK-2细胞内OPA1的表达变化及rhEPO干预的影响

Expression of optic atrophy 1 in renal tubular epithelial cells with hypoxia/re-oxygenation and the interventional effects of rhEPO

目的探讨重组人促红细胞生成素(recombinant human erythropoietin,rhEPO)干预对缺氧复氧后HK-2细胞内视神经萎缩症蛋白(optic atrophy 1,OPA1)表达变化及细胞凋亡率的影响。方法体外培养HK-2细胞随机分为正常对照组、H/R组和rhEPO干预组。然后免疫组化检测各组细胞胞质内OPA1蛋白表达变化,流式细胞仪检测各组细胞凋亡数量差异。结果与正常对照组比较,H/R组细胞数量减少,细胞凋亡率显著增加,同时细胞内OPA1表达减少;而与H/R组相比,rhEPO干预组细胞数量增加,细胞凋亡率下降,OPA1表达明显增强,但各指标仍未恢复至正常对照组水平。结论rhEPO对缺氧-复氧所致肾小管上皮细胞损伤具有保护作用,其机制可能通过抑制细胞内OPA1蛋白表达而实现。

Objective To investigate the expression of optic atrophy 1（OPA1）in renal tubular epithelial cells with hypoxia/re-oxygenation（H/R）and to evaluate the effects of recombinant human erythropoietin（rhEPO）on it. MethodsThe cultured human kedney proxiamal tubular cell-2（HK-2）cells in vitro were randomly divided into the following groups：normal control group,H/R group and rhEPO group.The expression of OPA1 protein was detected by immunohistochemistry,the rate of apoptosis cells was detected by flow cytometry. Results Compared with control group,the change in morphology of HK-2was most serious and obvious,and the apoptosis rate of cells was obviously increased and the expression of OPA1 was significantly decreased in H/R group.But compared with H/R group,the expression of OPA1 were significantly increased in rhEPO group and the apoptosis rate of cells were decreased. Conclusion RhEPO has protective effect on renal tubular epithelial cell injury induced by hypoxia/re-oxygenation,the mechanism may be achieved by inhibiting the expression of OPA1 protein in the cells.