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目的探讨冬凌草甲素(Oridonin)对人肺腺癌A549细胞凋亡的影响及其作用机制。方法采用MTT法观察不同浓度冬凌草甲素对A549细胞增殖的抑制作用;瑞氏-吉姆萨染色法检测细胞形态学的改变;Western blot法观察Bcl-2和Bax表达水平的变化。结果冬凌草甲素明显抑制A549细胞的增殖,作用24、48和72 h的IC50分别是87.9、67.6和45.2μmol/L,姬姆萨染色可观察到核染色质浓缩、胞浆空泡、核裂解等典型的凋亡细胞形态学改变,Western blot分析显示有Bcl-2表达的降低和Bax表达的上调。结论冬凌草甲素对人A549细胞具有生长抑制和诱导凋亡作用,同时抗凋亡蛋白Bcl-2表达的降低和促凋亡蛋白Bax上调可能是冬凌草甲素诱导肺腺癌A549细胞发生凋亡的重要作用机制之一。
Objective To investigate the effect of Oridonin on the apoptosis of human lung adenocarcinoma A549 cells and its mechanism. Methods MTT assay was used to observe the inhibitory effect of oridonin on proliferation of A549 cells. Wright-Giemsa staining was used to detect the morphological changes of cells. Western blot was used to observe the expression of Bcl-2 and Bax. Results Oridonin significantly inhibited the proliferation of A549 cells. The IC50 values at 24, 48 and 72 h were 87.9, 67.6 and 45.2 μmol / L, respectively. The chromatin condensation, cytoplasmic vacuolation, Typical morphological changes of apoptotic cells such as nuclear lysis were detected by Western blot analysis, with a decrease in Bcl-2 expression and an up-regulation of Bax expression. Conclusion Oridonin can inhibit the growth and induce apoptosis of A549 cells. The decrease of Bcl-2 protein expression and the up-regulation of Bax protein expression may be caused by oridonin inducing lung adenocarcinoma A549 cells One of the important mechanisms of apoptosis occurs.