P38MAPK在双氢青蒿素诱导Lewis肺腺癌细胞凋亡中的作用

Role of P38MAPK in Mediating Dihydroartemisinin-induced Apoptosis in Lewis Lung Carcinoma Cells

目的探讨p38丝裂素活化蛋白激酶(mitogen-activated protein kinases,MAPK)在双氢青蒿素(dihydroartemisinin,DHA)所致小鼠Lewis肺腺癌(Lewis lung carcinoma,LLC)细胞凋亡中的作用。方法以DHA处理LLC细胞后,采用四甲基偶氮唑盐(microculture terazolium,MTT)法观察LLC细胞增殖情况,采用流式细胞仪检测细胞周期和凋亡率,采用透射电镜观察凋亡细胞的形态,应用Western blot法检测p38MAPK表达及SB202190对其表达的影响。结果 DHA抑制LLC细胞增殖具有剂量效应关系,能使LLC细胞周期阻滞于G0/G1期;经20μg/ml DHA处理后,透射电镜下可见典型的凋亡细胞,Western blot显示p38MAPK表达阳性,并能被SB202190所抑制。结论 p38MAPK的活化参与了DHA诱导LLC细胞凋亡的过程。

Objective To study the role of p38MAPK in mediating Dihydroartemisinin （DHA）-induced apoptosis in Lewis lung carcinoma （LLC） cells. Methods After the treatment of DHA, proliferation activity of LLC cells was ob- served by MTT assay, cell cycle and apoptotic rate were detected by flow cytometry, the morphology of apoptotic ceils was observed by transmission electron microscopy, the expression of p38MAPK in LLC cells and the effect of SB202190 on p38MAPK expression were detected by Western blot. Results The proliferation activity of LLC cells was inhibited by DHA in a dose-dependent manner.The cell cycle of LLC cells was blocked in G0/G1 phase by DHA.After the treatment of 20t^g/ml DHA,the apoptotic cells were observed by transmission electron microscopy, p38MAPK positive signal which can be inhibited by SB202190 was found by Western blot. Conclusion The activation of p38MAPK participates in DHA- induced apoptosis in LLC cells.