卡维地洛对病毒性心肌炎心肌细胞凋亡及慢性期胶原重塑的干预作用及其机制的实验研究  

Effectand Mechanism of Carvedilol on Myocardial Cell Apoptosis of Viral Myocarditis and Chronic Phase Collagen Remodeling

作　　者：刘春梅[1] 路明[1] 

机构地区：[1]徐州医学院附属医院儿科,江苏徐州221000

出　　处：《标记免疫分析与临床》2015年第10期1033-1036,共4页Labeled Immunoassays and Clinical Medicine

摘　　要：目的探讨卡维地洛对病毒性心肌炎心肌细胞凋亡及慢性期胶原重塑的干预作用及其机制。方法将140只雄性BALb/c小鼠随机分为模型组(60只)、治疗组(60只)和对照组(20只)。模型组和治疗组小鼠给予腹腔注射CVB3,建立模型。治疗组于注射病毒1h后给予卡维地洛1.0 mg/kg/d。在接种21d后检测基质金属蛋白酶(MCP-1),肿瘤坏死因子α(TNF-α),一氧化氮合酶(i NOS),核因子κB(NF-κB)表达水平以及心肌细胞间质胶原容积分数(CVF)和细胞凋亡率(Rapo),测量各组小鼠的血压和心脏的质量及体质量;对比分析各组小鼠的心脏组织切片。结果 21d后模型组存活33只,治疗组存活44只,对照组全部存活,三组间具有统计学差异(χ2=15.082,P<0.01)。模型组和治疗组小鼠MCP-1,TNF-α,i NOS,NF-κB表达水平显著高于对照组(P<0.01),且治疗组显著低于模型组(P<0.01)。治疗后心肌细胞凋亡率和CVF显著高于对照组(P<0.01),且治疗组显著低于模型组(P<0.01)。结论卡维地洛可以有效降低病毒性心肌炎的炎性因子并以此达到保护心肌细胞、促进胶原重塑的作用。Objective To explore the intervention effect and mechanism of carvedilol on cardiomyocyte apoptosis in viral myocarditis and chronic collagen remodeling. Methods 140 male BALb/c mice were randomly divided into model group（60 rats） , treatment group （60 rats）and control group （20 rats）. The model group and the treatment group were treated with intraperitoneal injection of CVB3 to establish the experimental model. The treatment group was injected with 1 mg/kg earvedilol per day after 1 hour of virus injection. The expression level of MCP- 1, TNF- a, iNOS, NF- KB, CVF and Rapo in treatment group after 21 days were detected. The blood pressure, body weight and heart weight of mice were measured. The severity of myocarditis was assessed. Results After 21d, the survival of mice in model group was 33, the treatment group was 44, and the control group was all alive. There was a significantly difference on the survival between three groups（x= = 15. 082 ,P 〈 0. O1 ）. The expression levels of MCP- 1, TNF- oL, iNOS, NF- KB in the model group and the treatment group were significantly higher than those in the control group（ P 〈 0.01 ） , and the treatment group was significantly lower than that in the model group（P 〈0.01 ）. The apoptosis rate and CVF in model and treatment groups were significantly higher than that of the control group（ P 〈 0.01 ）, and the treatment group was significantly lower than that in the model group（ P 〈 0.01 ）. Conclusion The earvedilol could effectively reduce the inflammatory factor of viral myocarditis to protect myocardial cells and promote the collagen remodeling.

关 键 词：病毒性心肌炎 卡维地洛 细胞凋亡 胶原重塑 

分 类 号：R542.21[医药卫生—心血管疾病]