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目的:探讨信号转导和转录激活子3(STAT3)在病毒性心肌炎(VMC)发病机制中的作用。方法:以柯萨奇病毒B3感染balb/c小鼠,建立急慢性VMC的系列动物模型;经组织病理学方法证实模型后,采用免疫印迹法(Western blot)和免疫组化检测心肌组织细胞质和细胞核中STAT3和磷酸化STAT3(p-STAT3)蛋白。结果:Western-blot和免疫组化法显示柯萨奇病毒B3感染小鼠心肌细胞核STAT3和p-STAT3蛋白含量较对照组明显增高(P<0.05)。细胞质STAT3和p-STAT3蛋白含量与对照组比较差异无统计学意义(P>0.05)。结论:VMC时心肌细胞核STAT3和p-STAT3蛋白明显增高,与其发病密切相关。
Objective: To investigate the role of signal transducer and activator of transcription 3 (STAT3) in the pathogenesis of viral myocarditis (VMC). Methods: Balb / c mice were infected with coxsackievirus B3 (BALB / c) mice to establish a series of acute and chronic VMC models. After the model was confirmed by histopathology, Western blot and immunohistochemistry were used to detect the changes of cytoplasm STAT3 and phospho-STAT3 (p-STAT3) proteins in the nucleus. Results: Western-blot and immunohistochemistry showed that the content of STAT3 and p-STAT3 protein in myocardium of Coxsackie virus B3 infected mice was significantly higher than that of the control group (P <0.05). The contents of STAT3 and p-STAT3 in cytoplasm were not significantly different from those in control group (P> 0.05). CONCLUSION: STAT3 and p-STAT3 protein in myocardium are significantly increased in VMC, which is closely related to their pathogenesis.