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目的探讨高糖作用的肾小球系膜细胞ERK1/2蛋白表达与泛素-蛋白酶体调节途径的关系。方法体外培养大鼠肾小球系膜细胞,将高糖作为刺激因子,特异性泛素蛋白酶体抑制剂MG132作为干预因素。用蛋白免疫印迹法检测各组系膜细胞ERK1/2的表达,细胞免疫荧光染色及激光共聚焦显微镜检测各组系膜细胞ERK1/2的表达、转位。结果高糖组系膜细胞ERK1/2表达较正常血糖组均增多(P<0.05),还可促进ERK1/2由胞浆向胞核内激活、转位,高糖组加入MG132后,系膜细胞ERK1/2表达和激活、转位均减弱(P<0.05)。结论高糖可通过泛素蛋白酶体途径诱导肾系膜细胞ERK1/2表达增强和ERK1/2由胞浆向胞核内激活、转位。
Objective To investigate the relationship between ERK1 / 2 protein expression and ubiquitin - proteasome pathway in glomerular mesangial cells. Methods Rat glomerular mesangial cells were cultured in vitro. High glucose as a stimulating factor and specific ubiquitin proteasome inhibitor MG132 were used as intervention factors. The expression of ERK1 / 2 was detected by Western blotting. The expression of ERK1 / 2 and the translocation of mesangial cells were detected by immunofluorescence staining and confocal laser scanning microscopy. Results The expression of ERK1 / 2 in mesangial cells of high glucose group was higher than that of normal blood glucose group (P <0.05), and also promoted the activation and translocation of ERK1 / 2 from the cytoplasm to the nucleus. After MG132 was added into high glucose group, ERK1 / 2 expression and activation, translocation were weakened (P <0.05). Conclusion High glucose can induce ERK1 / 2 expression in mesangial cells through ubiquitin proteasome pathway and ERK1 / 2 activation and translocation from cytoplasm to nucleus.