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目的研究花旗松素对人肺癌细胞A549增殖的抑制作用,并探讨其诱导细胞凋亡的可能机制。方法 WST-1法检测不同质量浓度(0~200μg/m L)花旗松素对A549细胞增殖的影响;Annexin-V/PI双染法检测花旗松素对A549细胞凋亡的影响;细胞免疫荧光法观察花旗松素处理后A549细胞中凋亡蛋白Bax的表达;Western blotting法检测Bcl-2、Akt、P53蛋白表达的变化。结果 WST-1法检测到花旗松素能有效抑制A549细胞的增殖,呈现时间–剂量–效应关系。通过流式细胞仪分析,花旗松素诱导细胞凋亡,上调了促凋亡蛋白Bax的表达,下调抗凋亡蛋白Bcl-2的表达,抑制Akt的过表达,并且促进P53的表达。结论花旗松素对A549细胞的增殖具有显著的抑制作用,其诱导的凋亡机制可能与Bcl-2、Akt相关信号通路的激活有关。
Objective To study the inhibitory effect of Taxifolin on the proliferation of human lung cancer cell line A549 and to explore its possible mechanism of inducing apoptosis. Methods WST-1 method was used to detect the effect of Taxifolin on the proliferation of A549 cells with different concentrations (0 ~ 200μg / mL). The apoptosis of A549 cells was detected by Annexin-V / PI double staining method. Cell immunofluorescence Method was used to observe the expression of Bax protein in A549 cells treated with Taxifolin; Western blotting was used to detect the expression of Bcl-2, Akt and P53 proteins. Results WST-1 assay showed that Taxifolin can effectively inhibit the proliferation of A549 cells in a time-dose-response relationship. By flow cytometry, Taxifolin induced apoptosis, up-regulated the expression of Bax, decreased the expression of Bcl-2, inhibited the overexpression of Akt, and promoted the expression of P53. Conclusions Taxifolin can significantly inhibit the proliferation of A549 cells. The mechanism of apoptosis induced by Taxifolin may be related to the activation of Bcl-2 and Akt signaling pathways.