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用流感病毒PR8株感染8～10周龄p53+/+小鼠和p53-/-小鼠,分别在病毒感染后第3天和第6天采取小鼠肺组织,用基因芯片技术检测肺组织中细胞凋亡相关基因的表达水平,并对差异基因进行分析。结果显示,在病毒感染后第6天,p53+/+小鼠与p53-/-小鼠相比,促进细胞凋亡的基因表达明显上调,而抑制细胞凋亡的基因表达下调。比较caspase家族基因表达变化的结果显示,caspase 3和caspase 7的表达明显上调,而caspase 1和caspase 4的表达有所下调。此外,参与调控细胞凋亡的p53靶基因的表达也有明显的变化。研究结果表明,p53可能通过引起细胞凋亡而起到抗流感病毒的作用。
The infected mice were infected with PR8 strain of influenza virus (8-8 weeks old), p53 + / + mice and p53 - / - mice respectively. Lung tissues of mice were collected on day 3 and 6 after virus infection. Apoptosis-related gene expression levels, and analysis of differential genes. The results showed that on the 6th day after virus infection, the gene expression of p53 + / + mice was significantly up-regulated compared with that of p53 - / - mice, while the gene expression of apoptosis-inhibiting genes was down-regulated. Comparing caspase family gene expression results showed that caspase 3 and caspase 7 expression was significantly increased, while caspase 1 and caspase 4 expression was down-regulated. In addition, the expression of p53 target genes involved in the regulation of apoptosis is also significantly changed. The results show that p53 may play an anti-influenza virus effect by causing apoptosis.