紫草素诱导肺腺癌A549细胞凋亡及其机制的研究

目的 研究紫草素(shikonin, SK)诱导肺腺癌A549细胞凋亡及其作用机制。方法 不同浓度紫草素作用于肺腺癌A549细胞后,CCK-8法检测细胞的增殖情况；DAPI荧光染色法和FCM检测细胞凋亡；Western blotting检测紫草素处理48h后Bax、Bcl-2、p-Akt、p-ERK1/2的蛋白水平。结果 紫草素显著抑制肺腺癌A549细胞的增殖活性(P<0.05),诱导细胞凋亡,与空白对照组比较,紫草素处理组Bax表达上调(P<0.05),Bcl-2、p-Akt、P-ERK1/2表达下调(P<0.05)。结论 紫草素可以显著抑制肺腺癌A549细胞增殖,诱导细胞凋亡,其机制可能与线粒体凋亡途径,PI3K/Akt信号通路和ERK 1/2信号通路有关。

Mechanisms of shikonin-induced apoptosis in lung adenocarcinoma A549 cells

ObjectiveTo investigate the effects of shikonin(SK) on apoptosis in human lung adenocarcinoma A549 cells and its underlying mechanism. Methods After treatment with SK at various concentrations for different times, the viabilities of A549 cells were examined by CCK-8 assay. Cell morphological changes were measured by DAPI staining. Cell apoptosis was analyzed by flow cytometry. The expressions of Bax, Bcl-2, p-Akt and p-ERK1/2 proteins were detected by Western blotting. ResultsThe CCK-8 assay showed that SK inhibited the proliferation of A549 cells in a dose-and time-dependent manner. Florescence microscope with DAPI staining showed apoptotic changes in A549 cells after treatment with SK. Compared with control group, the expression of Bax protein was up-regulated while the expressions of Bcl-2, P-Akt and P-ERK proteins were down-regulated(P<0.05). Conclusion The results suggest that SK may inhibit the growth of lung cancer A549 cells and induce apoptosis, and mitochondrial apoptosis pathway, PI3K/Akt pathway and ERK 1/2 pathway might be involved in the process.