论文部分内容阅读
目的:观察甲型流感病毒(H1N1)感染人肺癌细胞株(A549细胞株)后,木犀草素的作用并探讨其机制。方法:利用基因芯片技术观察木犀草素作用感染细胞后,凋亡信号通路中基因转录的变化。采用q RT-RCR法,测定各组细胞中Caspase-8、Caspase-3和Myd88的m RNA的变化。结果:基因芯片提示,与模型组比较,奥司他韦组和木犀草素组对差异表达基因Myd88、Casp3、Casp6、Casp7、Casp8、Casp9、TRAIL、IL1A、IL1B明显下调。q RT-RCR提示:与模型组比较,奥司他韦组和木犀草素组对差异表达基因Casp3、Casp8和Myd88明显下调。结论:在体外环境下,流感病毒H1N1感染A549细胞激活凋亡通路后,木犀草素能通过降低相关基因表达,干预细胞凋亡,发挥抑制流感病毒的作用。
Objective: To observe the effect of luteolin on the lung cancer cell line (A549 cell line) infected with influenza A virus (H1N1) and to explore its mechanism. Methods: The changes of gene transcription in apoptotic signaling pathway were observed after infected with luteolin by gene chip technique. The changes of m RNA of Caspase-8, Caspase-3 and Myd88 in each group were determined by q RT-RCR method. Results: Gene chips showed that compared with model group, the expression of Myd88, Casp3, Casp6, Casp7, Casp8, Casp9, TRAIL, IL1A and IL1B were significantly down-regulated in both oseltamivir and luteolin groups. q RT-RCR Tip: Compared with the model group, oseltamivir and luteolin groups significantly downregulated the differentially expressed genes Casp3, Casp8 and Myd88. CONCLUSION: In vitro, influenza virus H1N1 can activate A549 cells to activate apoptotic pathway. Luteolin can interfere with apoptosis by reducing the expression of related genes and exert its inhibitory effect on influenza virus.