莫诺苷减轻CVB3感染心肌细胞炎症损伤的作用及其机制研究  

Studies on the role and mechanism of morroniside in attenuating inflammatory injury of CVB3-infected cardiomyocytes

作　　者：李卫东[1] 沈玄洋 张美琪 谭文涛 蒋晓路 沈媛 文红福 LI Weidong;SHEN Xuanyang;ZHANG Meiqi;TAN Wentao;JIANG Xiaolu;SHEN Yuan;WEN Hongfu(Department of Emergency,The Affiliated Hospital of North Sichuan Medical College,Nanchong 637000,Sichuan,China)

机构地区：[1]川北医学院附属医院急诊医学科,四川南充637000

出　　处：《西部医学》2025年第3期332-337,共6页Medical Journal of West China

基　　金：四川省医学会医学科研课题立项(s22101)。

摘　　要：目的探讨莫诺苷(MR)对柯萨奇病毒B3(CVB3)引起的心肌损伤的保护作用及其机制。方法分离培养SD乳鼠心肌细胞,使用CVB3感染心肌细胞建立心肌炎症损伤模型。随机将心肌细胞分为5组:Control组、CVB3组、CVB3+MR(10、50和100μM)组。CCK-8检测心肌细胞活力,Western blot检测NOD样受体热蛋白结构域相关蛋白3(NLRP3)、含CARD的相关斑点样蛋白(ASC)、活化的含半胱氨酸的天冬氨酸蛋白水解酶1(Cleaved caspase-1)、Cleaved caspase-3、Cleaved caspase-9、B细胞淋巴瘤因子(Bcl-2)和Bcl-2相关蛋白(Bax)的表达。ELISA检测白介素1β(IL-1β)、白介素18(IL-18)、肌酸激酶同工酶(CK-MB)和心肌肌钙蛋白Ⅰ(cTnI)表达水平。结果MR对各剂量组心肌细胞活力的影响无统计学差异(P>0.05)。与Control组相比,CVB3组心损标志物CK-MB和cTnI以及炎症因子IL-1β和IL-18的表达增加(P<0.05);与CVB3组相比,CVB3+MR各剂量组上述指标均下降(P<0.05)。与Control组相比,CVB3组中NLRP3、ASC、Cleaved caspase-1、Cleaved caspase-3、caspase-9和Bax表达增加(P<0.05),Bcl-2表达降低(P<0.05);与CVB3组相比,CVB3+MR各剂量组Bcl-2表达有所增加,其他蛋白表达均下降(P<0.05)。结论MR可以减轻CVB3感染心肌细胞炎症损伤,其机制与抑制心肌焦亡、凋亡和炎症反应有关。Objective To investigate the protective effect of morroniside(MR)on myocardial injury induced by Coxsackievirus B3(CVB3)and its mechanism.Methods Cardiomyocytes from SD mice were isolated and cultured,and myocardial inflammatory injury model was established by infecting cardiomyocytes with coxsackievirus B3(CVB3).Cardiomyocytes were randomly divided into 5 groups:Control group,CVB3 group,and CVB3+MR(10,50,and 100μM)group.CCK-8 was used to detect cardiomyocyte viability,and Western blot was used to detect the expression of NLRP3,ASC,Cleaved caspase-1,Cleaved caspase-3,Caspase-9,Bcl-2,and Bax proteins.ELISA was used to detect IL-1β,IL-18,CK-MB IL-1β,IL-18,CK-MB and cTnI were detected by ELISA.Results There was no difference in the effect of MR's on cardiomyocyte viability in each dose group(P>0.05).The expression of cardiac damage markers CK-MB and cTnI as well as inflammatory factors IL-1βand IL-18 was increased in the CVB3 group compared with the Control group(P<0.05),and all of the above indicators were decreased in the CVB3+MR group compared with the CVB3 group(P<0.05).Compared with the Control group,the expression of NLRP3,ASC,Cleaved caspase-1,Cleaved caspase-3,caspase-9 and Bax was increased in the CVB3 group(P<0.05),and the expression of Bcl-2 was decreased in the CVB3+MR group(P<0.05),and compared with the CVB3 group,the expression of Bcl-2 was increased(P<0.05),and all other protein expressions decreased(P<0.05).Conclusion MR attenuates inflammatory injury in CVB3-infected cardiomyocytes by mechanisms related to the inhibition of myocardial charring,apoptosis,and inflammatory responses.

关 键 词：莫诺苷 NLRP3炎性小体 柯萨奇病毒B3 凋亡 病毒性心肌炎 

分 类 号：R542.21[医药卫生—心血管疾病]