目的 探討核苷酸結(jié)合寡聚化結(jié)構(gòu)域樣受體蛋白3（NLRP3）在柯薩奇B組3型病毒（CVB3）誘導(dǎo)的病毒性心肌炎中的作用。方法 40只6～8周齡BALB/c雄性小鼠使用隨機(jī)數(shù)字表法隨機(jī)分為對照組和病毒性心肌炎模型組，每組20只。對照組ip 0.1 mL生理鹽水，模型組ip 0.1 mL含有CVB3病毒（1×10⁶ PFU/mL）的病毒液進(jìn)行造模。造模第7天，處死所有小鼠。酶聯(lián)免疫吸附法（Elisa）檢測血清NLRP3、白介素（IL）-1β和IL-18炎癥因子。結(jié)果 模型組NLRP3、IL-1β和IL-18表達(dá)水平分別為（26.43±4.14）、（31.25±5.63）、（38.57±6.45） μg/L，顯著高于對照組的（4.53±1.06）、（6.35±1.24）、（7.83±1.36） μg/L（P<0.01）。模型組心肌炎評分為（2.36±0.27）分，顯著高于對照組的（0.18±0.04）分（P<0.01）。模型組心肌細(xì)胞NLRP3表達(dá)評分為（1.82±0.24）分，顯著高于對照組的（0.16±0.03）分（P<0.01）。相關(guān)性分析顯示模型鼠NLRP3與體質(zhì)量呈顯著負(fù)相關(guān)（r=-0.517，P<0.05），和心肌炎評分呈顯著正相關(guān)（r=0.624，P<0.05）。結(jié)論 NLRP3炎癥小體可能參與了柯薩奇B組3型病毒致小鼠病毒性心肌炎的的發(fā)生過程。

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 (1×10⁶ PFU/mL) virus solution for modeling. On the 7th 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.