腺病毒介导心脏特异性过表达RIP140对大鼠心脏功能及炎症通路的影响

发布时间：2018-11-12 15:40

【摘要】：目的探讨心脏组织特异性过表达受体相互作用蛋白140(receptor interacting protein 140,RIP140)对心脏功能及炎症通路的影响。方法大鼠心脏组织多点注射携带RIP140基因的腺病毒载体,使心肌组织过表达RIP140;免疫荧光验证RIP140蛋白在心脏组织中的过表达情况;超声心动图与血流动力学参数评估心脏功能;ELISA分析TNF-α、IL-2、IL-1β等炎症因子水平;Western blot分析p65、IκB-α的蛋白水平。结果腺病毒载体介导的外源基因RIP140可成功过表达于心脏组织,诱导心室扩张、左室射血分数下降、心功能受损,促进心肌组织TNF-α、IL-2、IL-1β炎症因子释放,p65蛋白入核、胞质IκB-α蛋白降解。结论腺病毒介导RIP140基因在心脏组织中的特异性过表达损伤心脏功能,激活NF-κB/p65炎症通路,促进炎症因子释放。
[Abstract]:Objective to investigate the effects of cardiac tissue specific overexpression receptor interaction protein 140 (receptor interacting protein 140 RIP140 on cardiac function and inflammatory pathway. Methods the adenovirus vector carrying RIP140 gene was injected into rat heart tissue at multiple sites, and the overexpression of RIP140 protein in cardiac tissue was verified by immunofluorescence, and the cardiac function was evaluated by echocardiography and hemodynamic parameters. ELISA was used to analyze the levels of TNF- 伪, IL-2,IL-1 尾 and other inflammatory cytokines.; Western blot was used to detect the protein level of p65 I 魏 B- 伪. Results Adenovirus-mediated exogenous gene RIP140 was successfully expressed in cardiac tissue, induced ventricular dilatation, decreased left ventricular ejection fraction, impaired cardiac function, and promoted the release of TNF- 伪 and IL-2,IL-1 尾 inflammatory factors. P65 protein entered the nucleus and the I 魏 B-伪 protein in the cytoplasm was degraded. Conclusion Adenovirus-mediated overexpression of RIP140 gene in heart damages cardiac function, activates NF- 魏 B/p65 inflammatory pathway and promotes the release of inflammatory factors.
【作者单位】：广州医科大学附属第二医院药学部;中山大学肿瘤防治中心药学部;中山大学药学院;
【基金】：国家自然科学基金资助项目(No 81402923)
【分类号】：R54

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