甘氨酸改善缺氧性MDCK细胞损伤的作用依赖于ERK1/2、Akt及p38MAPK信号通路
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国家自然科学基金面上项目(81070120);江苏省高校自然科学研究面上项目(12KJD320005)


ERK,Akt and p38MAPK are involved in the cytoprotective effect of glycine on hypoxic impair in MDCK cells
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    摘要:

    目的:建立犬肾细胞(Madin-Darby canine kidney,MDCK)细胞缺氧模型,进一步阐明甘氨酸对缺氧细胞增殖活性的影响及其作用机制-方法:将MDCK细胞置于体积分数为95% N2和5% CO2的有机玻璃调节性密闭容器中,分别培养24-36-48-72 或84 h,用四甲基偶氮唑盐(MTT)法检测甘氨酸对缺氧性损伤MDCK细胞增殖活性的影响-将MDCK细胞分为正常组-缺氧组和甘氨酸处理组,加药后孵育1-2 或3 h后,收集细胞总蛋白,用Western blot检测细胞外信号调节激酶(extracellular signal-regulated kinase 1 and 2,ERK1/2)-p38MAPK和Akt的磷酸化活性-结果:在所观察的所有缺氧时段内,MDCK细胞MTT活性均较正常对照组明显下降(P < 0.01)-加入甘氨酸后,缺氧24-36或48 h后细胞的增殖能力比缺氧组有明显增强,差异有统计学意义-在缺氧72 或84 h后,甘氨酸未能显示明显的保护作用-缺氧时ERK1/2和Akt的磷酸化活性明显降低,p38MAPK的磷酸化活性明显增高-将甘氨酸加入到缺氧细胞中,ERK1/2和Akt又重新被激活,p38MAPK被抑制-结论:甘氨酸可保护MDCK细胞免于早期缺氧性损伤,该作用可能通过激活ERK1/2和Akt,抑制p38MAPK而实现-

    Abstract:

    Objective:To investigate the effects of glycine on hypoxic impair in cells. Methods:MDCK cells were cultured in a modular incubator chamber full of 95% N2 and 5% CO2 in the presence or absence of glycine for 24 h,36 h,48 h,72 h and 84 h. We observed the effects of glycine on cellular proliferation under hypoxic conditions by MTT method. Western blot was used to detect the phosphorylation activities of ERK1/2,p38MAPK and Akt in cells. Results:The proliferation of MDCK cells cultured under hypoxic conditions decreased significantly,while the proliferation increased after glycine treatment. Protective effect of glycine on cells was found at 24 h,36 h and 48 h of hypoxia. Activation of p38MAPK and depression of ERK1/2 and Akt in MDCK cells were detected when oxygen was deprived. Treatment with glycine antagonized the hypoxia-induced phosphorylative changes in ERK1/2,Akt and p38MAPK. Conclusion:Glycine could protect MDCK cells from early hypoxic injury. Activation of ERK1/2 and Akt but suppression of p38MAPK may contribute to the cytoprotective mechanisms of glycine on hypoxic impair in MDCK cells.

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秦 霞,蒋 莉,张咏梅,陈 琪.甘氨酸改善缺氧性MDCK细胞损伤的作用依赖于ERK1/2、Akt及p38MAPK信号通路[J].南京医科大学学报(自然科学版),2012,(10):1337-1342

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  • 收稿日期:2012-04-29
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