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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 atorvastatin calcium treatment on the expression of matrix metalloproteinase-2 (MMP-2) and tissue inhibitor of metalloproteinase-2 (TIMP-2) and to explore the role of atorvastatin calcium in myocardial ischemia Possible mechanism of protective effect of blood reperfusion injury. Methods Rabbits were randomly divided into normal control group, ischemia reperfusion placebo group and atorvastatin calcium group. In the control group, the left anterior descending coronary artery of the control group underwent thoracotomy and did not ligate the thoracotomy. The other two groups were subjected to myocardial ischemia-reperfusion model by blocking the left anterior descending coronary artery with polyethylene tube and aseptic suture. 30 min ischemia and 180 min reperfusion. Calculate the extent of myocardial ischemia and myocardial infarction. The mean absorbance values were used to assess the expression of MMP-2 and TIMP-2. Results The range of myocardial ischemia was (38.61 ± 1.53)% in ischemia-reperfusion placebo group and (37.5 ± 1.5)% in atorvastatin calcium group, with no significant difference between the two groups (P> 0.05) The range of infarction was (50.00 ± 2.00)% in ischemic reperfusion placebo group and (29.67 ± 2.08)% in atorvastatin calcium group, with significant difference between the two groups (P <0.01). The expression of MMP-2 in ischemia / reperfusion placebo group (1.17 ± 0.09) was significantly higher than that in normal control group (0.23 ± 0.04) and atorvastatin calcium group (0.21 ± 0.03) (all P <0.05) The expression of TIMP-2 in statin group (0.24 ± 0.02) was significantly higher than that in normal control group (0.18 ± 0.04) and ischemia-reperfusion placebo group (0.17 ± 0.02) (all P <0.05). Conclusions Short-term calcium treatment with atorvastatin may exert myocardial protective effect by inhibiting the expression of matrix metalloproteinase-2 and increasing the expression of tissue inhibitor of metalloproteinase TIMP-2.