摘要
目的研究在病毒性心肌炎小鼠模型上敲减Itk蛋白的表达对小鼠炎症反应的影响。方法BALB/c小鼠尾静脉注射表达Itk-shRNA的质粒后感染CVB3,第4天后观察Itk基因的抑制情况、小鼠存活率,PBMC增殖率及部分炎症性细胞因子的分泌水平。结果Itk.shRNA转染至小鼠体内后脾细胞中Itk基因的mRNA水平与空白对照组及转染shRNAnon的对照组相比,敲减率约40%(P〈0.05)。与转染shRNAnon组相比,Itk-shRNA组中Itk基因表达的抑制导致小鼠PBMC增殖活性降低约41%,小鼠的存活率提高(P〈0.05)。Itk—shRNA组血清中细胞因子水平降低。结论抑制Itk表达能有效降低小鼠PBMC的增殖,同时减少炎症相关细胞因子的分泌,提高小鼠的存活率。
Objective To study the effect of Itk down regulation on PBMC cell proliferation and inflammatory cytokines production in a Coxsackievirus-induced myocarditis model. Methods BALB/c mice were injected via caudal vein with plasmid Itk-shRNA then infected with CVB3. The change of hk protein expression, cell proliferation, cytokines production and mice survival rate of mice were observed in the fourth days after infected. Results hk mRNA in groups of mice transfected with hk-shRNA was reduced about 40% in spleen cells, compared with that in control groups or shRNAnon groups (P 〈0. 05). PBMC proliferation and serum cytokines were significantly inhibited by transfected with hk-shRNA. Conclusion Knocking down Itk expression can inhibit mice inflammatory reaction.
出处
《中华实验和临床病毒学杂志》
CAS
CSCD
2012年第3期205-207,共3页
Chinese Journal of Experimental and Clinical Virology
基金
北京市自然科学基金(7102023)
北京市优秀人才资助项目(2011A003034000032)