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目的:观察RIP1/RIP3坏死体在柯萨奇病毒B3(CVB3)诱导的急性病毒性心肌炎中的表达及意义,探讨其特异性抑制剂Nec-1的心肌损伤保护作用。方法:40只雄性BALB/c小鼠,分为正常对照组(腹腔注射0.9%氯化钠溶液)、CVB3组(腹腔注射CVB3 4h后,尾静脉注射等剂量的DMSO)、Nec-1组(腹腔注射CVB3 4h后,尾静脉注射Nec-1)和空白对照组(无任何处理)。腹腔注射药物均连续7d。采用Western blotting及免疫组织化学技术对心脏标本RIP1/RIP3坏死体进行检测,并在光镜及电镜下观察Nec-1对小鼠心肌损伤的保护作用。结果:与对照组相比,CVB3组心肌组织RIP1和RIP3表达增加,Nec-1组较CVB3组明显降低(均P<0.01);Nec-l组小鼠心肌组织病变程度明显改善。结论:程序性坏死在CVB3诱导的急性病毒性心肌炎中起到重要作用,Nec-1能阻断这种作用并可能产生新的治疗方式。
Objective: To observe the expression and significance of RIP1 / RIP3 necrosis in CVB3-induced acute viral myocarditis and to explore the protective effect of its specific inhibitor Nec-1 on myocardial injury. Methods: Forty male BALB / c mice were divided into three groups: normal control group (0.9% sodium chloride solution), CVB3 group (4h after CVB3 intraperitoneal injection) and Nec-1 group After intraperitoneal injection of CVB3 for 4 hours, Nec-1 was injected into the caudal vein) and blank control group (without any treatment). Intraperitoneal injection of drugs were continuous 7d. Western blotting and immunohistochemistry were used to detect the necrosis of RIP1 / RIP3 in heart specimens. The protective effect of Nec-1 on myocardial injury was observed under light and electron microscope. Results: Compared with the control group, the expression of RIP1 and RIP3 in CVB3 group was significantly increased, while in Nec-1 group was significantly lower than that in CVB3 group (all P <0.01). The degree of myocardial lesions in Nec-1 group was significantly improved. Conclusion: Programmed necrosis plays an important role in CVB3-induced acute viral myocarditis. Nec-1 blocks this effect and may lead to new therapeutic approaches.