基础医学与临床 ›› 2014, Vol. 34 ›› Issue (10): 1372-1375.

• 研究论文 • 上一篇    下一篇

多巴胺受体2减轻离体大鼠心肌缺血/再灌注损伤

李鸿珠1,高君2,郝晓敏1,张丽敏1,陈俊亭1   

  1. 1. 哈尔滨医科大学
    2. 哈尔滨市第一医院
  • 收稿日期:2014-03-17 修回日期:2014-05-26 出版日期:2014-10-05 发布日期:2014-09-25
  • 通讯作者: 李鸿珠 E-mail:hongzhuli61@163.com
  • 基金资助:
    黑龙江省教育厅科学技术研究项目

DR2 attenuates myocardial ischemia/reperfusion injury of rats in vitro

  • Received:2014-03-17 Revised:2014-05-26 Online:2014-10-05 Published:2014-09-25
  • Contact: Hong-Zhu LI E-mail:hongzhuli61@163.com

摘要: 目的 观察多巴胺受体2(DR2)对离体大鼠心肌缺血/再灌注(I/R)损伤的影响及其可能机制。方法 将大鼠 40 只,每组n=10,随机分成对照组(control)、I/R组、10μmol/L Bromocriptine(DR2 激动剂)组(Bro),10μmol/L Haloperidol (DR2 抑制剂)组(Hal)。用 Langendorff离体灌流装置,复制大鼠心肌I/R损伤模型。Powerlab 生理记录仪记录心功能;比色法测定冠脉流出液 LDH、CK 活性和心肌组织匀浆 SOD 活性以及 MDA 含量;TUNEL 染色检测心肌细胞凋亡;Western blot检测DR2、Bcl-2、caspase-3和caspase-9蛋白的表达。结果 与对照组比较,I/R组DR2、Bcl-2、caspase-3和caspase-9蛋白表达、LDH和CK 活性、MDA 含量和细胞凋亡率均增加(P<0.01),唯有SOD活性降低,心功能减弱(P<0.01)。与I/R组比较,Bro 降低LDH和CK活性、MDA含量、细胞凋亡率、caspase-3和caspase-9的表达,升高SOD活性,改善心功能和进一步增加Bcl-2的表达(P<0.01);Hal 对上述指标影响不显著。结论 DR2可减轻心肌I/R损伤,其机制与抗氧化、清除自由基、上调Bcl-2表达以及下调caspase-3和caspase-9的表达有关。

关键词: 2类多巴胺受体, 缺血/再灌注损伤, 细胞凋亡, 大鼠, 心肌

Abstract: Objective To observe the effects of dopamine receptors-2 (DR2) on the myocardial ischemia/reperfusion (I/R) injury in rats and to study the possible mechanisms. Methods 40 Wistar rats were randomly divided into 4 groups (n=10): control group, I/R group, Bromocriptine group (Bro) and Haloperidol group (Hal). Myocardial ischemia/reperfusion injury of isolated rats was induced with Langendorff system; The heart function was recored by Powerlab; LDH, CK activities of coronary effluent and SOD activity and MDA content of myocardial tissue homogenate were measured by colorimetric method; Myocardial cell apoptosis was detected by TUNEL staining; The expression of DR2, Bcl-2, caspase-3 and caspase-9 was detected by Western blot. Results Compared with control group, the expressions of DR2, Bcl-2, caspase-3, caspase-9, the activity of LDH and CK, the MDA content, the rate of cell apoptosis were increased (P<0.01), but the SOD activity and heart function were decreased in the I/R group (P<0.01). Compared with I/R group, Bro decreased the activity of LDH and CK, the MDA content, the rate of cell apoptosis, the expression of caspase-3 and caspase-9, increased the SOD activity and Bcl-2 expressions, improved heart function (P<0.01). Hal did not change the above indexes. Conclusion Our results suggest that DR2 inhibites I/R injury through antioxidation, scavenging free radical, up-regulation of Bcl-2 expressions and down-regulation of caspase-3 and caspase-9 expressions.

Key words: dopamin receptors-2, ischemia/ reperfusion injury, apoptosis, Rats, myocardial

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