文章摘要
骨形态发生蛋白-2信号通路在右美托咪定所致大鼠房室结缝隙连接蛋白表达中的作用
Role of BMP-2 signaling pathway in the changes of expression of connexins in atrioventricular node induced by dexmedetomidine in rats
  
DOI:10.12089/jca.2019.12.017
中文关键词: BMP-2信号通路  右美托咪定  窦性心动过缓  缝隙连接蛋白
英文关键词: BMP-2 signaling pathway  Dexmedetomidine  Sinus bradycardia  Connexins
基金项目:贵州省科技厅联合资金(黔科合LH字〔2016〕7262)
作者单位E-mail
钟毅 550004,贵阳市,贵州医科大学附属医院麻醉科 490173559@qq.com 
祝瑜 湖北医药学院附属人民医院超声科  
路凯 贵州医科大学麻醉学院  
殷永强 贵州医科大学麻醉学院  
田磊 贵州医科大学麻醉学院  
安丽 550004,贵阳市,贵州医科大学附属医院麻醉科  
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中文摘要:
      
目的 探讨骨形态发生蛋白-2(BMP-2)信号通路在右美托咪定所致窦性心动过缓大鼠心脏房室结中缝隙连接蛋白Cx30.2、Cx40和Cx45表达中的作用。
方法 成年健康雄性SD大鼠30只,按随机数字表法分为三组,每组10只。对照组(C组)通过股静脉持续泵注与实验组等体积的生理盐水;右美托咪定组(D组)给予右美托咪定负荷量120 μg/kg于10 min内泵注完毕,持续泵注60 μg·kg-1·h-1共120 min;右美托咪定+Noggin组(DN组)先通过腹腔注射BMP-2信号通路特异性抑制剂Noggin 75 ng/kg,余同D组。记录大鼠心动过缓发生情况(HR下降幅度>基础值的30%、稳定30 min为模型制作成功)。观察结束后迅速开胸取出心脏准确分离房室结组织,采用Western blot法检测Cx30.2、Cx40、Cx45及BMP-2蛋白含量。
结果 D组Cx30.2、Cx45、BMP-2蛋白含量明显高于C组(P<0.05)。DN组Cx30.2、Cx45、BMP-2蛋白含量明显低于D组(P<0.05)。D组Cx40蛋白含量明显低于C组(P<0.05)。DN组Cx40蛋白含量明显高于D组(P<0.05)。
结论 BMP-2信号通路可能参与了右美托咪定所致窦性心动过缓模型大鼠房室结中缝隙连接蛋白表达的改变。
英文摘要:
      
Ojective To investigate the mechanism of BMP-2 signal pathway in the expression changes of gap junction protein Cx30.2, Cx40 and Cx45 in atrioventricular node of sinus bradycardia rats induced by dexmedetomidine.
Methods Thirty adult healthy male SD rats were randomly divided into three groups (n = 10). Control group (group C) received continuous infusion of normal saline of the same volume as the experimental group through femoral vein. Dexmedetomidine given group (group D) was pumped a loading dose of 120 μg/kg within 10 mins, then continuously infused 60 μg·kg-1·h-1 for 120 mins. In Dexmedetomidine + Noggin group (group DN): a loading dose of 120 μg/kg dexmedetomidine was pumped within 10 min after intraperitoneal injection of “Noggin” 75 ng/kg, a specific inhibitor of BMP-2 signaling pathway, then continuous pump volume of 60 μg·kg-1·h-1 dexmedetomidine was injected for 120 min. In the course of the experiment, the occurrence of bradycardia in the three groups was recorded (the decrease of HR was more than 30% as the basic HR and keeping stable for 30 min was considered to be a successful model). At the end of the observation, the heart was removed from the chest and the atrioventricular node tissue was separated accurately. The expression of Cx30.2, Cx40, Cx45 and BMP-2 protein was detected by Western blot, respectively.
Results The expression of Cx30.2, Cx45 and BMP-2 protein in group D was significantly higher than that in group C (P < 0.05). The expression of Cx30.2, Cx45 and BMP-2 protein in group DN was significantly lower than that in group D (P < 0.05). The expression of Cx40 protein in group D was significantly lower than that in group C (P < 0.05). The expression of Cx40 in group DN was significantly higher than that in group D (P < 0.05).
Conclusion BMP-2 signaling pathway is involved in the changes of Cx30.2, Cx40 and Cx45 expression in the atrioventricular node of rats with dexmedetomidine-induced sinus bradycardia.
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