核因子-κB活化在小鼠CVB_3病毒性心肌炎的病理作用机制研究

Nuclear factor κB activation and mechanism on myocardium of CVB 3 myocarditis in Balb/c mice

目的观察Balb/c小鼠CVB3病毒性心肌炎心肌组织核因子-κB活化的动态变化并探索其病理机制。方法采用CVB3感染Balb/c小鼠,分别于感染后2h、第3、7、14、21天取其心肌,采用凝胶滞留分析法检测NF-κB活性、TUNELassay检测心肌组织细胞凋亡,测定心肌组织Caspase3酶活性。结果小鼠感染CVB3后NF-κB迅速活化,并呈持续性活化状态,主要是P65-P50二聚体活化。TUNEL检测细胞凋亡发现病毒感染第7天病灶内炎症细胞凋亡,至第15、21天心肌细胞凋亡。Caspase3酶活性在病毒感染后第7天开始升高,第14、21天明显升高。结论NF-κB活化在病毒性心肌疾病的病理机制中,对炎症反应与细胞凋亡的调控均起重要作用。

Objective To investigate the activation of transcription factor, nuclear factor kappa-B （NF-B）, and to assess its functional role s in the evolution of CVB 3 myocarditis in Balb/e mice. Methods Balb/c mice were inoculated intraperitoneally with CVB 3. And the activation of NF- κB were clarified by electrophoretic mobility shift assays （EMSA）, apoptosis by TUNEL assays, activation of caspase 3 and histopathology were evaluated at 2 hours and 3 rd, 7 th and 21 st day postinfection. Results NF-kB, especially P65-P50 heterodimer were activated rapidly and persisted after CVB 3 inoculation in BALB/c mice. Inflammatory cells apoptosis were found in cardiac tissue at 7 th day. The activation of caspase 3 began to appear at 7 th day and increasing at 15 th and 21 st days postinfection. Conclusion NF-kB activation plays an important role in the cardiac myocyte inflammation and apoptosis on CVB 3 myocarditis in Balb/c mice.