MAPKs信号通路在镉致大鼠大脑皮质神经细胞毒性中的作用  

The effect of cadmium on MAPKs activities of rat primary cerebral cortical neuron cultured invitro

作　　者：江辰阳[1] 徐卉[1] 胡飞飞[1] 张康保[1] 袁燕[1] 刘学忠[1] 卞建春 刘宗平[1] 

机构地区：[1]扬州大学兽医学院,江苏扬州225009

出　　处：《中国兽医学报》2014年第4期628-632,共5页Chinese Journal of Veterinary Science

基　　金：国家自然科学基金资助项目(31101866);江苏高校优势学科建设工程资助项目

摘　　要：为了研究MAPKs信号通路在镉致大鼠大脑皮质神经细胞毒性中的作用,对体外培养的神经细胞用不同浓度醋酸镉(0、5、10、20μmol/L)作用12h,通过免疫组化和免疫印迹法检测了MAPK蛋白磷酸化水平,Hoechst 33258荧光染色观察细胞核形态的变化。结果表明,与对照组相比,各染毒组细胞ERK、JNK、p38MAPK的磷酸化水平随染毒剂量增加而显著升高(P<0.05或P<0.01),细胞核出现固缩浓染、碎裂等典型的凋亡特征。说明MAPKs信号通路激活在镉致大鼠大脑皮质神经细胞毒性中发挥作用。To investigate the effect of cadmium on MAPK activities in rat primary cerebral cortical neurons cultured in vitro. After the cells were exposured to cadmium acetate at different concen- trations（0,5,10,20 μmol/L） for 12 h,immunohistochemistry and Western blot were used to de- tect the phosphorylation levels of the MAPK proteins, Hoechst staining was used to detect the morphological changes of nucleus. In comparison with the control group, the results showed that the phosphorylation levels of ERK,JNK and p38 MAPK increased significantly with increasing the higher concentration cadmium acetate（P〈0.05 or P〈0.01）,the typical morphological changes of apoptosis were observed in neurons, such as nucleus crimpled and disintegrated. It was suggested that cadmium induces the activation of MAPK proteins in rat primary cerebral cortical neurons culture.

关 键 词：镉 大脑皮质神经细胞 ERK JNK P38MAPK 

分 类 号：S856.9[农业科学—临床兽医学]