氨基胍抑制氧化应激致细胞骨架蛋白羰基化  

Amino guanidine inhibit the carbonylation of cytoskeleton protein induced by oxidative stress

作　　者：张秋生[1] 张猛[1] 黄贤键[1] 刘晓佳[1] 李维平[1] 

机构地区：[1]深圳市第二人民医院,深圳518035

出　　处：《浙江创伤外科》2015年第6期1079-1082,共4页Zhejiang Journal of Traumatic Surgery

基　　金：深圳市协同创新计划国际科技合作项目(GJHZ20120614154914623);深圳神经外科学重点实验室(ZDSYS20140509173142601)

摘　　要：目的探讨氧化应激对细胞骨架羰基化的作用及机制,并观察羰基化抑制剂氨基胍对细胞氧化损伤的抑制作用。方法应用0、100、200、300μmol/L的H2O2干预PC12细胞系建立细胞氧化损伤模型,测定GSH、脂质过氧化反应产物(Thiobarbituric acid reactive substance,TBARS)浓度,pull-down/Western blot检测细胞骨架蛋白β-actin和β-tubulin羰基化水平和溶解度。氨基胍预处理PC12细胞,检测其对β-actin和β-tubulin羰基化损伤的抑制作用。结果 H_2O_2处理后,PC12产生氧化损伤,β-actin和β-tubulin发生羰基化反应,骨架蛋白溶解度增高,氨基胍可抑制细胞骨架蛋白的羰基化,差异具有统计学意义(P<0.05)。结论氧化应激损伤导致细胞骨架蛋白羰基化反应会破坏细胞骨架蛋白的稳定性,氨基胍可有效抑制氧化应激导致的羰基化反应。Objective To investigate the carbonylation of cytoskeleton protein and the effect of amino guanidine on the inhibition of cy-toskeleton carbonylation induced by oxidative damage. Methods PC12 cell line was intervention by H2O2（with concentration of 0, 100, 200 and300 umol/L）to establish oxidative damage model, the concentration of GSH, lipid peroxidation products（thiobarbituric acid reactive substance,TBARS）were detected, and pull-down/Western blot was used to detect the carbonylation, solubility of β-actin andβ-tubulin. Then, amino guanidine was used to inhibition the carbonylate of β-actin and β-tubulin. Results The content of GSH and MDA were significantly changed after intervented by H2O2,the carbonylation and solubility of β-actin and β-tubulin were significantly higher in H2O2 dealed PC12 cell line（P 〈0.05）. Amino guanidine can inhibit the carbonylation of cytoskeletal protein, with a statistically significant difference（ P〈0.05）. Conclusion Oxidative stress can induced the carbonylation of cytoskeleton protein and destroy the stability of cytoskeleton protein, amino guanidine can effectively inhibit this oxida-tive stress.

关 键 词：蛋白质羰基化 氧化应激 颅脑创伤 氨基胍 

分 类 号：R687.3[医药卫生—骨科学]