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作 者:张飞 王娟 ZHANG Fei;WANG Juan(Department of Emergency,Wuhan Central Hospital of Tongji Medical College of Huazhong University of Science and Technology,Wuhan 430000,China)
机构地区:[1]华中科技大学同济医学院附属武汉中心医院急诊科
出 处:《药物评价研究》2019年第12期2360-2363,共4页Drug Evaluation Research
摘 要:目的探讨核苷酸结合寡聚化结构域样受体蛋白3(NLRP3)在柯萨奇B组3型病毒(CVB3)诱导的病毒性心肌炎中的作用。方法 40只6~8周龄BALB/c雄性小鼠使用随机数字表法随机分为对照组和病毒性心肌炎模型组,每组20只。对照组ip 0.1 mL生理盐水,模型组ip 0.1 mL含有CVB3病毒(1×10^6PFU/mL)的病毒液进行造模。造模第7天,处死所有小鼠。酶联免疫吸附法(Elisa)检测血清NLRP3、白介素(IL)-1β和IL-18炎症因子。结果模型组NLRP3、IL-1β和IL-18表达水平分别为(26.43±4.14)、(31.25±5.63)、(38.57±6.45)μg/L,显著高于对照组的(4.53±1.06)、(6.35±1.24)、(7.83±1.36)μg/L (P<0.01)。模型组心肌炎评分为(2.36±0.27)分,显著高于对照组的(0.18±0.04)分(P<0.01)。模型组心肌细胞NLRP3表达评分为(1.82±0.24)分,显著高于对照组的(0.16±0.03)分(P<0.01)。相关性分析显示模型鼠NLRP3与体质量呈显著负相关(r=-0.517,P<0.05),和心肌炎评分呈显著正相关(r=0.624,P<0.05)。结论NLRP3炎症小体可能参与了柯萨奇B组3型病毒致小鼠病毒性心肌炎的的发生过程。Objective To detect the role of NLRP3 in coxsackievirus induced viral myocarditis. Methods Forty BALB/c male mice aged 6 一 8 weeks were randomly divided into control and viral myocarditis model groups, each group had 20 mice. The control group were ip 0.1 mL normal saline, and the model group were ip containing CVB3 virus(1×10^6 PFU/mL) virus solution for modeling. On the 7 th day, all mice were killed. Elisa was used to detect serum NLRP3, IL-1β, and IL-18 inflammatory factors.Results The expression levels of NLRP3, IL-1β and IL-18 in model group were(26.43 ± 4.14),(31.25 ± 5.63) and(38.57 ± 6.45)μg/L, which was significantly higher than that of(4.53 ± 1.06),(6.35 ± 1.24) and(7.83 ± 1.36) μg/L in control group(P < 0.01). The myocarditis score of model group was(2.36 ± 0.27), which was significantly higher than that of(0.18 ± 0.04) in control group(P <0.01). The NLRP3 score of model group was(1.82 ± 0.24), which was significantly higher than that of(0.16 ± 0.03) in control group(P < 0.01). NLRP3 was negatively correlated with body weight(r =-0.517, P < 0.05) and positively correlated with myocarditis score(r = 0.624, P < 0.05). Conclusion NLRP3 inflammatory bodies may be involved in the pathogenesis and development of viral myocarditis in mice induced by Coxsackie B virus type 3.
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