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目的:研究姜黄素对急性心肌梗死模型大鼠的保护作用并探讨其机制。方法:结扎冠状动脉前降支以复制大鼠急性心肌梗死模型。100只SD大鼠分为假手术(ig,等容生理盐水)组、模型(ig,等容生理盐水)组、溶剂对照[ip,6%乙醇-聚乙二醇400溶液,2.5 ml/kg]组、培哚普利(ig,3 mg/kg)组与姜黄素高、中、低剂量(ip,200、100、50 mg/kg)组,复制模型24 h后开始给药,每天1次,连续4周。测定大鼠血液动力学指标[左室舒张末压(LVEDP)、左室收缩末压(LVSP)、左室内压最大上升/下降速率(±dp/dtmax)];计算左、右心室质量指数(LVMI、RVMI);计算心肌梗死面积(IS),测定心肌胶原面积并计算心肌胶原容积分数(CVF);采用免疫组化法测定大鼠心肌基质金属蛋白酶(MMP)-2的表达。结果:与假手术组比较,模型组大鼠LVSP、±dp/dtmax降低、LVEDP、LVMI、RVMI升高,IS增加,CVF升高,MMP-2表达增强,差异有统计学意义(P<0.01)。与模型组比较,姜黄素高、中、低剂量组大鼠LVSP、±dp/dtmax升高,LVMI、RVMI降低,CVF降低,MMP-2表达减弱;姜黄素高、中剂量组大鼠LVEDP降低,差异有统计学意义(P<0.01或P<0.05)。结论:姜黄素对急性心肌梗死模型大鼠具有一定保护作用,其机制可能与减轻心肌肥厚、减少胶原沉积、降低MMP-2的表达有关。
Objective: To study the protective effect of curcumin on acute myocardial infarction (AMI) model rats and to explore its mechanism. Methods: Ligation of the anterior descending coronary artery to replicate acute myocardial infarction model in rats. 100 SD rats were divided into sham operation group (ig, isosceles saline group), model group (ig, isosceles saline group), solvent control [ip, 6% ethanol- (Ip, 200, 100 and 50 mg / kg) groups were treated with perindopril (ig, 3 mg / kg) and curcumin Times, for 4 weeks. Left ventricular end-diastolic pressure (LVEDP), left ventricular end-systolic pressure (LVSP), and maximum ± dp / dtmax of left ventricular pressure were measured; the left and right ventricular mass index LVMI and RVMI). The area of myocardial infarction (IS) was calculated. The area of myocardial collagen was measured and the myocardial collagen volume fraction (CVF) was calculated. The expression of matrix metalloproteinase (MMP) -2 was detected by immunohistochemistry. Results: Compared with sham operation group, LVSP, ± dp / dtmax, LVEDP, LVMI and RVMI increased, IS increased, CVF increased, MMP-2 expression increased in model group ). Compared with model group, LVSP, ± dp / dtmax, LVMI, RVMI, CVF and MMP-2 in curcumin group were significantly decreased , The difference was statistically significant (P <0.01 or P <0.05). CONCLUSION: Curcumin has a protective effect on rats with acute myocardial infarction. Its mechanism may be related to reducing cardiac hypertrophy, reducing collagen deposition and decreasing the expression of MMP-2.