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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 inhibi-ting endoplasmic reticulum stress.