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目的:探讨亚麻木酚素(SDG)联合蛋白酶体抑制剂硼替佐米(Bortezomib,Bor)对肺腺癌A549细胞凋亡的影响及其机制。方法:MTT法检测细胞增殖;Annexin V-FITC/PI双染流式细胞法和Hoechst 33258荧光染色法检测细胞凋亡;比色法检测半胱氨酸天冬氨酸蛋白酶-3(Caspase-3)活性;Real Time PCR检测Caspase-3、BCL-2、BAXmRNA的表达;Western Blot检测BCL-2、Bax及p-JNK的蛋白表达。结果:SDG联合Bor能明显抑制细胞生长,上调Caspase-3活性,促进p-JNK、BAX mRNA和蛋白的表达,抑制BCL-2 mRNA和蛋白的表达,诱导细胞凋亡。结论:SDG联合Bor可显著诱导肺腺癌A549细胞的凋亡,其机制可能与其激活JNK信号通路有关。
AIM: To investigate the effect and mechanism of Bortezomib (Bor) on the apoptosis of human lung adenocarcinoma A549 cells by lincomycin (SDG) combined with proteasome inhibitor. Methods: Cell proliferation was detected by MTT assay. Apoptosis was detected by Annexin V-FITC / PI double staining flow cytometry and Hoechst 33258 staining. Caspase-3 ) Activity. The expression of Caspase-3, BCL-2 and BAX mRNA was detected by Real Time PCR. The protein expressions of BCL-2, Bax and p-JNK were detected by Western Blot. Results: SDG combined with Bor could significantly inhibit the cell growth, upregulate the activity of Caspase-3, promote the expression of p-JNK, BAX mRNA and protein, inhibit the expression of BCL-2 mRNA and protein, and induce apoptosis. Conclusion: SDG combined with Bor can significantly induce the apoptosis of lung adenocarcinoma A549 cells, which may be related to its activation of JNK signaling pathway.