线粒体氯通道蛋白在过氧化氢诱导C6细胞损伤中的作用

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:500 μmol/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1000 μmol/L H2O2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H₂O₂诱导神经胶质瘤细胞损伤的机制。

Role of mtCLIC/CLIC4 in injured C6 glioma cells induced by hydrogen peroxide

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 increased 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.