EGCG抑制内质网应激减轻高糖致HK-2细胞凋亡的作用  

Mechanism of EGCG protecting high-glucose-induced HK-2 cell apoptosis by suppressing endoplasmic reticulum stress

作　　者：项春红 吕丽[2] 江蓓[1] 肖晓燕[1] 胡昭[1] 

机构地区：[1]山东大学齐鲁医院肾内科,山东济南250012 [2]内蒙古科技大学包头医学院第一附属医院肾内科,内蒙古包头014010

出　　处：《山东大学学报（医学版）》2017年第12期1-6,共6页Journal of Shandong University:Health Sciences

基　　金：中国博士后科学基金面上项目(2015M572048);齐鲁医院临床研究项目(2014QLKY13)

摘　　要：目的探究表没食子儿茶素没食子酸酯(EGCG)对高糖环境下人肾小管上皮细胞(HK-2)的保护作用。方法根据高糖可诱导HK-2细胞损伤将细胞分为正常糖组、甘露醇组、高糖组及不同浓度的EGCG组,干预HK-2细胞24 h后,采用CCK8法检测HK-2细胞的增殖。Hoechst33258染色和Annexin V法检测正常糖组、甘露醇组、高糖组、(20μmol/L)EGCG组作用24 h后HK-2细胞凋亡;Western blotting检测上述4组HK-2细胞内质网应激反应蛋白GRP78和Caspase-12蛋白的表达。结果高糖组培养HK-2细胞24 h后,细胞增殖较正常糖组明显降低,细胞凋亡较正常糖组明显增加(P<0.001)。(20μmol/L)EGCG组干预24 h后能明显改善高糖环境下HK-2细胞的增殖。EGCG(20μmol/L)作用24 h后能明显降低细胞的凋亡率(P<0.001),且EGCG干预后内质网应激反应蛋白GRP78和Caspase-12蛋白表达较高糖组也明显降低(P=0.001)。结论 EGCG可能通过抑制内质网应激介导的凋亡途径改善高糖致HK-2细胞的凋亡。Objective To investigate the protective effect and mechanism of epigallocatechin 3-gallate（ EGCG） on HK-2 cells exposed to high glucose. Methods The HK-2 cells were divided into normal glucose group,mannitol group,high glucose group,and EGCG group. After 24-hour treatment,cell proliferation was measured with CCK8;cell apoptosis was measured with Hoechst33258 and Annexin V staining; the expressions of GRP78 and Caspase-12 were determined with Western blotting. Results Compared with the normal glucose group,the high glucose group showed significantly inhibited cell proliferation and increased apoptosis（ P〈0. 001）,while the EGCG（ 20 μmol/L）group displayed significantly improved cell proliferation,reduced apoptosis rate（ P〈0. 001）,and decreased GRP78 and Caspase-12 expressions（ P = 0. 001）. Conclusion EGCG may reduce high-glucose-induced HK-2 apoptosis by inhibiting endoplasmic reticulum stress.

关 键 词：表没食子儿茶素没食子酸酯 内质网应激 人肾小管上皮细胞 细胞凋亡 

分 类 号：R692.6[医药卫生—泌尿科学]