首页|阿托伐他汀钙短期预处理对兔心肌缺血再灌注损伤的保护作用

阿托伐他汀钙短期预处理对兔心肌缺血再灌注损伤的保护作用

Cardioprotective effect of short-term atorvastatin calcium preconditioning on myocardial ischemia reperfusion injury rabbits model

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目的 观察阿托伐他汀钙短期预处理在调节心肌基质金属蛋白酶-2(MMP-2)、组织金属蛋白酶抑制剂-2(TIMP-2)表达中的作用,探讨阿托伐他汀钙发挥心肌缺血再灌注损伤保护作用的可能机制.方法 将兔随机分为正常对照组、缺血再灌注安慰剂组和阿托伐他汀钙组.正常对照组开胸后冠状动脉左前降支下穿一线,不结扎;另两组开胸后采用聚乙烯小管与无菌缝线阻断冠状动脉左前降支血流建立心肌缺血再灌注模型,进行30 min缺血和180 min再灌注.计算心肌缺血范围和心肌梗死范围.采用平均吸光度值评估MMP-2、TIMP-2的表达水平.结果 心肌缺血范围在缺血再灌注安慰剂组为(38.61±1.53)%,阿托伐他汀钙组为(37.5±1.5)%,两组间差异无统计学意义(P>0.05);心肌梗死范围在缺血再灌注安慰剂组为(50.00±2.00)%,阿托伐他汀钙组为(29.67±2.08)%,两组间差异具有统计学意义(P<0.01).缺血再灌注安慰剂组MMP-2的表达(1.17±0.09)显著高于正常对照组(0.23±0.04)与阿托伐他汀钙组(0.21±0.03)(均P<0.05);阿托伐他汀钙组TIMP-2的表达(0.24±0.02)显著高于正常对照组(0.18±0.04)与缺血再灌注安慰剂组(0.17±0.02)(均P<0.05).结论 阿托伐他汀钙短期预处理可能通过抑制基质金属蛋白酶MMP-2的表达、上调组织金属蛋白酶抑制物TIMP-2的表达发挥心肌保护作用.
Objective To observe the effect of short-term pretreatment with atorvastatin calcium on regulating expression of matrix metalloproteinase-2 ( MMP-2) and tissue inhibitor of metalloproteinase-2 (TIMP-2) in myocardial ischemia reperfusion injury rabbits model. Methods The rabbits were randomly divided into normal control group, placebo group, atorvastatin calcium group. Myocardial ischemia reperfusion injury model was built according to traditional methods. After ischemia 30min, then reperfusion 180min, the area of ischemic and infarcted myocardium was evaluated via TTC staining, the expression level of MMP-2 and TIMP-2 in ischemia/reperfusion myocardium were evaluated via mean optical density. Result the area of ischemic myocardium of atorvastain calcium group (37.5 ±1.50) wasn' t signifcantly different from placebo group (38. 61 ± 1. 53), but the infarcted area (29. 67 ±2. 08) was significantly lower than that of placebo group (50.00±2.00) (P < 0.01). The expression level of MMP-2 in myocardial cytoplasm was signifcantly higher in placebo group (1.17 ±0.09) than normal control group(0.23 ± 0.04) and atorvastatin calcium group (0.21 ±0.03) (all P <0.05). But the expression level of TIMP-2 was signifcantly higher in atorvastatin calcium group (0. 24 ±0.02) than placebo group (0. 17 ±0. 02) ( P <0.05). Conclusion The cardioprotective mechanism of atorvastation calcium on myocardial ischemia reperfusion injury maybe involved in inhibiting the expression of MMP-2 and upregulating the expression of T1MP-2.

atorvastatin calciuischemia reperfusion injurypreconditioningmetalloproteinase 2tissue inhibitor of metalloproteinase 2rabbits

徐卫亭、李渊、赵良平、陈建昌、尤涛、肖飞、王诗俊

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苏州大学附属第二医院心内科,江苏苏州215004

阿托伐他汀钙 缺血再灌注损伤 预处理 基质金属蛋白酶-2 组织金属蛋白酶抑制剂-2

苏州市科技发展计划指导项目

SYSD2010125

2012

苏州大学学报(医学版)
苏州大学

苏州大学学报(医学版)

CSTPCD
影响因子:0.499
ISSN:1673-0399
年,卷(期):2012.32(2)
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