【摘要】 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。更多还原

【Abstract】 Objective:To observe the role of luteolin and explore its mechanism after the infection of influenza A virus(H1N1) in human lung cancer cell line(A549 cell line).Methods:The chips were used to screen the differentially expressed genes which selected from the apoptotic signaling pathway.The m RNA expressions of Casp3,Casp8 and Myd88 were verified by q RTPCR.Results:According to the gene chips,oseltamivir and luteolin could down-regulate the expressions of Casp3,Casp6,Casp7,Casp8,Casp9 and MYD88 compared with the virus-infected group.q RT-PCR experiments showed that luteolin could significantly decrease the expressions of Casp3,Casp8 and MYD88.Conclusion:When apoptosis of A549 cells infected by influenza virus in vitro were induced,luteolin could down-regulate the expressions of genes related to the apoptosis pathway,which could interfere the cell apoptosis induced by virus infection,so as to achieve the anti-virus action.更多还原