论文部分内容阅读
目的:研究牡丹苷A对人肺癌A549细胞株的作用以及其诱导人肺癌A549细胞株凋亡机制。方法:本研究采用MTT法检测牡丹苷A对体外人肺癌细胞株A549增殖率的影响。Annexin V/PI双标法检测牡丹苷A对A549凋亡率,蛋白免疫印迹法和细胞免疫细胞化学法分别检测牡丹苷A对A549细胞株PI3K,Akt,NF-κBp65,Bax,Bcl-2的表达,并采用PI3K/Akt/NF-κB通路的激动剂IGF-1和抑制剂wortmannin进一步探讨牡丹苷A对PI3K/Akt/NF-κB信号通路的作用。结果:牡丹苷A能够抑制A549的增殖,上调Bax蛋白的表达量,下调Bcl-2蛋白的表达量,Bcl-2/Bax比值显著降低,同时降低PI3K,NF-κBp65的蛋白表达,抑制Akt磷酸化。结论:牡丹苷A能够阻碍A549增殖,并促进其凋亡,其诱导凋亡的机制可能与抑制PI3K/Akt/NF-κB通路有关。
Objective: To study the effect of beindin A on human lung cancer cell line A549 and its mechanism of apoptosis in A549 human lung cancer cell line. Methods: The purpose of this study was to determine the effect of betanin A on the proliferation of human lung cancer cell line A549 in vitro by MTT assay. Annexin V / PI double staining was used to detect the apoptosis rate of A549 by beinosine A. Western blot and immunocytochemistry were used to detect the inhibitory effect of betanin A on the expressions of PI3K, Akt, NF-κBp65, Bax and Bcl-2 in A549 cells And the effect of peonyidin A on the PI3K / Akt / NF-κB signaling pathway was further explored by using the agonist IGF-1 of PI3K / Akt / NF-κB pathway and inhibitor wortmannin. Results: Beyenin A could inhibit the proliferation of A549, up-regulate the expression of Bax protein, down-regulate the expression of Bcl-2 protein, decrease the Bcl-2 / Bax ratio and decrease the protein expression of PI3K and NF-κBp65, The Conclusions: Bendin A can inhibit the proliferation of A549 and promote its apoptosis. The mechanism of its induction may be related to the inhibition of PI3K / Akt / NF-κB pathway.