p38 MAPK、Caspase-s介导PTH诱导PC12细胞凋亡机制的研究附视频

被引:1
作者
李冬冬
王婧一
李悦
安惠霞
机构
[1] 哈尔滨医科大学附属第二医院肾内科
关键词
甲状旁腺激素; PC12细胞; 凋亡; p38 MAPK; Caspase-3;
D O I
暂无
中图分类号
R692.5 [肾功能衰竭];
学科分类号
100221 [泌尿外科学];
摘要
目的甲状旁腺激素(PTH1-34)对PC12细胞作用和p38MAPK、Caspase-s在PTH1-34对PC12细胞凋亡中作用机制。方法应用CCK-8法测定PTH对PC12细胞生长抑制率,通过细胞形态学、乳酸脱氢酶(LDH)和流式细胞仪方法检测细胞损伤,RT-PCR测定p38 mRNA的表达,通过Western blot检测细胞中p38磷酸化丝裂原活化蛋白激酶(MAPK)及caspase-3蛋白的变化。结果 CCK-8法测定PTH抑制PC12细胞生长;透射电镜可见细胞核呈固缩状、凋亡小体出现等典型的凋亡形态学改变;流式细胞仪可见细胞凋亡率增多;LDH渗出量增多等。PTH1-34可明显上调p38 mRNA的表达,并可明显地促进PC12细胞磷酸化p38MAPK与Caspase-3的蛋白表达。结论 PTH可诱导PC12细胞凋亡,p38MAPK和Caspase-s共同介导参与PTH致PC12细胞凋亡。
引用
收藏
页码:410 / 414
页数:5
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