胰岛素样生长因子1对缺氧复氧诱导的HK-2细胞损伤作用  

Protective effects of IGF-1 on HK-2 cells with hypoxia-reoxygenation injury and the possible mechanism

作　　者：袁海[1] 张琦[1] 杨开智[1] 张军伟[2] 

机构地区：[1]湖北省襄樊市中心医院肾病内科,441021 [2]华中科技大学同济医学院2006级硕士研究生

出　　处：《临床肾脏病杂志》2010年第1期32-34,共3页Journal Of Clinical Nephrology

摘　　要：目的探讨胰岛素样生长因子1（IGF-1）对缺氧复氧损伤人肾近曲小管上皮细胞株HK-2的凋亡影响及其作用机制。方法将体外培养的HK-2细胞分为正常对照组（A组）、缺氧复氧损伤模型组（B组）、提前IGF-1干预组（C组）、即时IGF-1干预组（D组）、迟后IGF-1干预组（E组）5组。3个IGF-1干预组在不同时间给予IGF-1干预，复氧培养24h后，MTT比色法检测细胞增殖活性，流式细胞仪分析细胞凋亡，细胞免疫组织化学法检测Bcl—2阳性表达变化，Real-time PCR检测Bcl-2 mRNA表达水平变化。结果与A组相比，B组细胞增殖活性明显降低（P〈0．05），细胞凋亡率明显升高（P〈0．05），Bcl-2蛋白与Bcl-2 mRNA表达明显降低（P〈0．05）；与B组比较，IGF-1干预后，细胞增殖活性有所升高，以C组升高最明显（P〈0．01），细胞凋亡率显著下降（P〈0．05），又以C组下降最明显（P〈0.01）；Eel-2mRNA和其蛋白表达量均增高（P〈0．05），以C组表达量增高最明显（P〈0.01）。结论IGF-1能够抑制缺氧复氧损伤HK-2细胞凋亡，可能与其上调Bcl—2蛋白表达有关。Objective To investigate the protective effect of IGF-1 on HK-2 cells induced by hypoxia-reoxygenation and the possible mechanisms. Methods Cultured HK-2 cells in vitro were divided into 5 groups as follows： control group （group A）, hypoxia-reoxygenation group （group B）, prehopoxia IGF-I interfering group （group C）, simultaneous IGF-1 interfering （group D）, and post hypoxia IGF-1 interfering group （group E）. Each group underwent hypoxia reoxygenation except for group A. The cells in groups C,D,and E were incubated with IGF-1 at different time points. Twentyfour h after reoxygenation, cell proliferation activities were detected by MTT colorimetry, apoptosis rate by flow cytometry, and the expression of Bcl-2 by immunohistochemstry and real-time PCR. Resuits As compared with group A, cell proliferation activity and the expression of Bcl-2 were significantly reduced （P〈0. 05）, but apoptosis rate increased in group B（P〈0. 05）. All of these changes were reduced by IGF-1 interference,with the most significant extent in group C. Conclusion IGF-1 inhibits the apoptosis of HK-2 cells induced by hypoxia reoxygenation injury possibly by up-regulating the expression of Bcl-2 protein.

关 键 词：胰岛素样生长因子1 缺血再灌注损伤 细胞凋亡 

分 类 号：R587.1[医药卫生—内分泌] R692.6[医药卫生—内科学]