摘要
目的:利用过氧化氢(H2O2)复制神经胶质瘤C6细胞损伤模型,探讨线粒体氯通道蛋白/CLIC4的变化。方法:应用MTT法检测H2O2作用的C6细胞生存率;紫外分光光度法检测培养液上清LDH释放率;RT-PCR检测CLIC4的mRNA表达;Western blotting方法检测CLIC4的蛋白水平。结果:500μmol/L H2O2作用C6细胞存活率与对照组相比未见明显差异;LDH释放率高于对照组;CLIC4蛋白水平明显强于对照组。而1000μmol/LH2O2作用的C6细胞存活率明显低于对照组;LDH释放率明显高于对照组;CLIC4蛋白水平强于对照组。结论:CLIC4可能参与HO诱导神经胶质瘤细胞损伤的机制。
AIM： To explore the changes and the possible function of mtCLIC/CLIC4 （mitochondrial chloride intracellular channel 4） proteins in malignant C6 glioma cells treated with hydrogen peroxide （ H2O2 ）. METHODS： The viability of C6 cells was measured by MTT assay, LDH release rate was detected by ultraviolet spectrophotometry, CLIC4 mRNA level was determined by RT- PCR and CLIC4 protein level was measured by Western blotting. RESULTS： Compared with the control group, the cell viability was constant, the LDH release rate increased obviously, and the CLIC4 protein level also inereased significantly in 500 μmol/L H2O2 treated group （P 〈0. 05, respectively）. However, the cell viability decreased, LDH release rate increased significantly （P 〈 0. 01, respectively）, and the CLIC4 protein level increased obviously in 1 000 μmol/L H2O2 treated group （P 〈0. 05）. CONCLUSION： The CLIC4 protein may be involved in the process of C6 injuries induced by H2O2.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2008年第3期481-483,共3页
Chinese Journal of Pathophysiology
基金
国家自然科学基金资助项目(No.30570687)
