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首页> 中文期刊> 《中国药理学通报》 >JNK信号通路介导化学性缺氧对PC12细胞的损伤作用

JNK信号通路介导化学性缺氧对PC12细胞的损伤作用

         
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Aim To investigate the role of C-Jun N-terminal kinase ( JNK ) in PC 12 cell injury induced by Cobalt chloride ( CoCl2 ). Methods PC12 cells were treated with Cobalt chloride ( CoCl2 ) to set up a chemical hypoxia-induced cellular injury model. Cell viability was tested by cell counter kit ( CCK-8 ); Cell apopto-sis was observed by Hoechst33258 staining and photo-fluorography; Mitochondria! Membrane potential ( MMP ) was determined by JC-1 staining followed by photofluorography; Phosphorylation of JNK was measured by western blot assay. Results From 12 to 48 h, CoCl2 time-dependently inhibited cell viability in PC 12cells. Treatment with CoCl2 at 600 jjumol ? L"1 for 48 h induced PC 12 cell apoptosis and decreased MMP. CoCl2 upregulated JNK phosphorylation. SP600125 , a specific blocker of JNK significantly inhibited CoCl2-induced PC 12 cell injury. Conclusion CoCl2 may induce PC 12 cell injury. This effect may be associated with the CoCl2-induced activation of JNK.%目的 探讨C-Jun蛋白氨基末端激酶(C-Jun N-terminal kinase,JNK)通路在化学性缺氧模拟剂氯化钴(CoCl2)对PC12细胞损伤中的作用.方法 应用化学性低氧模拟剂氯化钴(CoCl2)处理PC12细胞以建立化学性缺氧损伤模型.应用CCK-8比色法检测细胞存活率;Hoechst33258核染色法观察细胞凋亡的形态学改变;JC-1染色荧光显微镜照像检测线粒体膜电位(MMP); Western blot法检测JNK蛋白的表达水平.结果 600 μmol·L-1 CoCl2作用PC12细胞不同时间(12～48 h)后,可时间依赖性地抑制PC12细胞的存活率;600 μmol·L-1的CoCl2处理PC12细胞48 h时,可引起细胞出现核固缩等典型的凋亡特征;CoCl2能明显的降低PC12细胞的MMP; CoCl2能诱导JNK的磷酸化,特异性的JNK阻断剂SP600125可抑制CoCl2对PC12细胞的上述损伤作用.结论 CoCl2可引起PC12细胞损伤,此作用可能与其诱导JNK磷酸化有关.

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