番荔枝内酯对肺腺癌A549细胞周期及凋亡的影响

目的：探讨番荔枝内酯 Bullatacin 诱导肿瘤细胞凋亡的机制。方法采用 MTT 法检测不同浓度（6.25、12.5、25、50、100μg/mL）Bullatacin对A549细胞的抑制增殖作用,依照MTT结果取浓度25μg/mL Bullatacin作用于A549细胞0、12、24、48 h,流式细胞仪分析其对A549细胞增殖周期的影响,观察其对细胞凋亡的干预作用。Western Blot 检测不同实验组 ERK、JNK、p38磷酸化与总蛋白的表达。结果不同浓度Bullatacin作用于A549细胞后,呈明显的剂量依赖性；25μg/mL Bullatacin能将A549细胞周期阻滞在G0/G1期,诱导细胞凋亡；与空白组比较,P-ERK、P-JNK、P-p38的蛋白表达均明显增强。结论 Bullatacin明显抑制A549细胞增殖,并诱导其凋亡,其机理与Bullatacin通过磷酸化各蛋白激酶而激活MAPK通路有关。

Effects of Bullatacin on Proliferation and Apoptosis of A549 Cell Line of Pulmonary Adenocarcinoma

Objective To investigate the apoptosis induction of Bullatacin on A549 cell line of pulmonary adenocarcinoma. Methods The MTT assay was used to detect the growth inhibition rates of A549 cells cultured with Bullatacin in different concentrations （6.25, 12.5, 25, 50, 100μg/mL）. 25μg/mL Bullatacin was used to culture A549 cells for 0, 12, 24, 48 h. The cell cycle distribution and apoptosis were measured by flow cytemetry. The protein expressions of ERK, JNK, and p38 were studied by Western blot. Results Dosage dependence was obviously showed after the different concentrations of Bullatacin were used to A549, and 25 μg/mL;Bullatacin blocked A549 cell in G0/G1 periods and induced its apoptosis. Compared with the blank group, protein expressions of P-ERK, P-JNK, and P-p38 were all increased by different degrees. Conclusion Bullatacin significantly inhibits the proliferation and induces the apoptosis of A549 cell. Its mechanism is related to activity of MAPK pathway thought the phosphorylation of the three protein kinases by Bullatacin.