摘要
目的探讨泛素蛋白酶体途径对高糖刺激的肾系膜细胞IκB-α蛋白表达的影响。方法体外培养大鼠HBZY-1肾系膜细胞,高糖作为刺激因子,MG132作为干预因素。分别设正常对照组、高糖组(10,20,30mmol/L葡萄糖)、甘露醇组以及MG/32加高糖(30mmol/L)组,分别作用12、24、48小时,用Western blot法测各组IκB-α蛋白的表达。结果 (1)与正常对照组比较,高糖作用后IκB-BRA蛋白的表达呈时间、浓BZ度依赖性下降。(2)与高糖组比较,高糖加入MG132后,IκB-α蛋白的表达下降被明显逆转。结论高糖可通过泛素蛋白酶体途径促进肾系膜细胞IJLB-α蛋白泛素化降解。
Objective To explore the effect of high glucose and MG132 on the protein expression of IκB-a in cultured rat glomerular mesangial cells(GMC). Methods The cultured HBZY-1 rat GMC were divided into 7 groups(MG132, a proteasome inhibitor): normal glucose (5.6mmol/L) group,high glucose (10,20,30mmol/L) group, mannitol(24.6mmol/L) group, MG132 plus 30mmol/L glucose group, MG132 plus 5.6mmol/L glucose group. The expression of IκB-a was measured by Western-blot. Results 1. Compared with normal glucose group, the expression of IκB-a was decreased significantly in high glucose groups in a dose- and time-dependent manner (all P〈0. 05). 2. Compared with 30mmol/L high glucose group, the expression of IκB-a could be reverted mostly by adding the MG132 (P〈0. 01). Conclusions High glucose can increase significantly the degradation of IκB-a in cultured GMC. Degradation of IκB-a induced by high glucose is related with ubiquitin-proteasome pathway.
出处
《中国糖尿病杂志》
CAS
CSCD
北大核心
2009年第6期447-448,共2页
Chinese Journal of Diabetes
基金
国家自然科学基金资助项目(30670980)
四川省杰出青年基金资助项目(08ZQ026-026)
关键词
糖尿病肾病
高糖
肾系膜细胞
IκB-a
泛素蛋白酶体途径
Diabetic nephropathy
High glucose
Glomerular mesangial cell
IκB-a
Ubiquitin- proteasome pathway