高糖诱导人肾近曲小管上皮细胞凋亡及其调控机制  

Apoptosis of HK-2 cells induced by high glucose and its regulation mechanism

作　　者：袁育珺[1] 段惠芳[2] 胡志坚[1] 汪渊[3] 

机构地区：[1]九江学院附属医院检验科,九江332000 [2]九江学院附属医院医保办,九江332000 [3]安徽省/省部共建教育部重要遗传病基因资源利用重点实验室,合肥230032

出　　处：《安徽医科大学学报》2016年第4期497-501,共5页Acta Universitatis Medicinalis Anhui

基　　金：国家自然科学基金(编号:81272399)

摘　　要：目的研究高糖诱导人肾近曲小管上皮细胞凋亡及其调控机制。方法以人肾近曲小管上皮细胞株HK-2为研究对象,随机分为对照组、高糖组、甘露醇组。MTT、流式细胞术观察细胞的增殖和凋亡状况;ELISA法检测细胞内C.aspase的活性;Westem blot法分析B淋巴细胞瘤-2(B1-2)及Caspase家族蛋白的表达变化。结果与对照组比较,高糖组能抑制HK-2细胞的体外增殖,下调抑制凋亡作用的蛋白Bcl-2表达,上调促凋亡作用的蛋白Bax、Bak表达(P<0.05);流式细胞术显示HK-2细胞周期有明显的变化,且随葡萄糖浓度的升高中期凋亡和末期凋亡所占的比例明显上升(P<0.01),并且Caspase酶原降解及活性表达也呈上升趋势(P<0.01)。结论高糖能抑制HK-2细胞体外增殖,并诱导其凋亡,其机制可能是通过Bcl-2及Caspase家族调控HK-2细胞的凋亡。Objective To investigate high glucose-induced apoptosis in HK-2 cells and its possible regulation mechanism. Methods HK-2 cells were divided into three groups and treated as follows： normal group, high glu- cose groups, mannitol groups. The cell proliferation and apoptosis of HK-2 cell was analyzed by MTF, flow cytome- try. The expression of Bcl-2 and Caspase family proteins were studied by Western blot, and the activity of Caspase family was analyzed by ELISA. Results High glucose could inhibit growth of HK-2 cells. Moreover, high concen- trations of glucose could also induce apoptosis with the concentration increased more obviously（P 〈 0. 01 ）. Western blot showed that high glucose down-regulated Bcl-2, increased Bak, Bax expression （P 〈 0. 05 ）. Conclusion High glucose can inhibit the proliferation of HK-2 cells in vitro and induce its apoptosis , and its mechanism may regulate the apoptosis of HK-2 ceils through Bcl-2 and Caspase families.

关 键 词：高糖 HK-2 凋亡 表达 

分 类 号：R735.7[医药卫生—肿瘤]