P44/42MAPK介导雷公藤甲素致肾上腺皮质细胞凋亡作用简

目的：了解P44/42丝裂素活化蛋白激酶在雷公藤甲素诱导大鼠肾上腺皮质细胞凋亡中的作用。方法：体外分离培养大鼠肾上腺皮质细胞,以不同浓度梯度雷公藤甲素染毒相同时间,或相同浓度雷公藤甲素染毒不同时间,以蛋白因子添加素V和碘化丙啶联合标记,流式细胞仪检测细胞凋亡率;蛋白印迹法分析P44/42总蛋白量、磷酸化水平以及c-Fos的表达水平。结果：雷公藤甲素以时间和剂量依赖的方式诱导细胞凋亡;雷公藤甲素诱导P44、P42磷酸化水平升高及c-Fos的高表达。结论：一定剂量雷公藤甲素作用于肾上腺皮质细胞后,P44/42过度磷酸化,诱导c-Fos的高表达,导致细胞凋亡。

Effect of Apoptosis on Adrenocortical Cells Induced by Triptolide through P44/42MAPK

Objective：To study the role of P44/42MAPK on the apoptosis of adrenocortical cells of rat induced by Triptolide. Methods ： Adrenocortical cells of rats were dispersed primarily in vitro, with different concentration gradients of Triptolide poisoning at the same time, or in the same concentration of Triptolide poisoning at different time points, using combined labeling with annexin-V and propidium iodide （ PI ） and flow cytomelry, the protein imprinting method analysis to detect the total protein, phosphorylation level and c-Fos expression level. Results ： The average percentage of apoptotic cells increased with dosage or duration of Triptolide. Triptolide could remarkably increase the phosphorylation levels of P44 and P42, and the expression level of c-Fos. Conclusions ： Triptolide could induce apoptosis of adrenocortical cells through the over-phosphorylated P44/42 and the over-expression of e-Fos in turn.