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目的探讨融合蛋白Pep-1-vMIP-Ⅱ在影响宿主ARGs基因表达抵抗HIV-Ⅰ感染中的作用。方法小鼠背部涂抹Pep-1-vMIP-Ⅱ2 h后,用免疫组织化学方法测定不同组织器官中vMIP-Ⅱ的穿膜情况。用实时定量PCR,检测24 h后不同组织器官中ARGs mRNA表达水平;用Graphpad Prism 5软件分析实验数据。结果皮肤涂抹Pep-1-vMIP-Ⅱ组2 h后vMIP-Ⅱ在肾脏分布明显增加(P<0.05);涂抹Pep1-vMIP-Ⅱ24 h后,白细胞、肾、心、肝和肺中CCL5的mRNA表达水平有明显差异(P<0.05),脑组织中CCL5的表达未见明显增加;MX1、MX2在多种组织中都表达上调(P<0.05)。结论Pep-1-vMIP-Ⅱ可以穿透小鼠皮肤进入肾脏组织,主要通过激活CCL5基因表达发挥调控作用。
Objective To investigate the role of fusion protein Pep-1-vMIP-Ⅱ in affecting host ARGs gene expression in HIV-I infection. Methods After mice were smeared with Pep-1-vMIP-Ⅱ for 2 h, the transmembrane morphology of vMIP-Ⅱ in different tissues and organs was determined by immunohistochemistry. Real-time quantitative PCR was used to detect the mRNA expression of ARGs in different tissues and organs after 24 hours. The experimental data were analyzed by Graphpad Prism 5 software. Results The distribution of vMIP-Ⅱ in the skin of Pep-1-vMIP-Ⅱ group was significantly increased in the kidney (P <0.05). After 24 hours of Pep1-vMIP-Ⅱ treatment, the expression of CCL5 mRNA in leukocytes, kidney, heart, liver and lung (P <0.05). There was no significant increase in CCL5 expression in brain tissue. MX1 and MX2 were up-regulated in many tissues (P <0.05). Conclusion Pep-1-vMIP-Ⅱ can penetrate the skin of mice and enter the kidney tissue, which plays a regulatory role mainly through the activation of CCL5 gene expression.