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目的:通过大鼠心肌缺血再灌注损伤(IRI)模型,分析白细胞介素-17(IL-17)在IRI中的作用。方法:用阻断大鼠冠状动脉左前降支的方法制作IRI模型。Realtime-PCR及Western blot方法动态观察IRI后不同时间点心肌组织IL-17的表达水平,流式细胞术进一步检测IL-17的来源。应用抗IL-17抗体体内干预,观察其对IRI的作用。结果:IRI后1h就有IL-17的表达,并且在24h的观察期内持续存在,未有峰值出现。流式细胞术检测结果显示心肌组织中IL-17的主要来源是CD4+T细胞。用抗IL-17的抗体体内干预后,血清肌钙蛋白T的水平降低,心肌梗死面积也明显减小。结论:IL-17参与大鼠IRI过程,中和IL-17能明显减轻心肌IRI。
Objective: To investigate the role of interleukin-17 (IL-17) in IRI by myocardial ischemia-reperfusion injury (IRI) in rats. Methods: The IRI model was made by blocking the left anterior descending coronary artery in rats. Realtime-PCR and Western blot methods were used to dynamically observe the expression of IL-17 in myocardium at different time points after IRI. The origin of IL-17 was further detected by flow cytometry. In vivo intervention with anti-IL-17 antibody was used to observe its effect on IRI. Results: The expression of IL-17 was detected at 1 hour after IRI and persisted within the observation period of 24 hours. No peak appeared. Flow cytometry results showed that the main source of IL-17 in myocardium was CD4 + T cells. After in vivo intervention with an anti-IL-17 antibody, serum troponin T levels decreased and myocardial infarct size was significantly reduced. Conclusion: IL-17 is involved in the process of IRI in rats, neutralizing IL-17 can significantly reduce myocardial IRI.