瑞舒伐他汀对心肌肥厚大鼠心肌组织MMP-2和MMP-9蛋白表达的影响

目的：探讨瑞舒伐他汀对心肌肥厚大鼠心肌组织基质金属蛋白酶（MMP）-2和MMP-9的影响。方法：40只远交群（SD）大鼠随机分为正常对照组、模型组、卡托普利组和瑞舒伐他汀组，每组10只。模型组、卡托普利组和瑞舒伐他汀组大鼠皮下注射异丙肾上腺素制作心肌肥厚大鼠模型，正常对照组同期皮下注射生理盐水。模型制作成功后，瑞舒伐他汀组给予瑞舒伐他汀4mg／kg，每日1次灌胃；卡托普利组予卡托普利60mg／kg，每日1次灌胃，其他两组均给予等量生理盐水。4周后测定4组全心质量指数（全心湿质量与体质量比）、左心室质量指数（左心室湿质量与体质量比），采用分光光度法检测左心室心肌组织胶原含量，免疫组织化学法检测MMP-2、MMP-9蛋白的表达水平。结果：模型组大鼠的心肌肥厚指数、胶原含量及MMP-2和MMP-9蛋白的表达水平均明显高于对照组（P〈0．05），瑞舒伐他汀组和卡托普利组大鼠心肌组织胶原含量、MMP-2及MMP-9蛋白的表达明显低于模型组（P〈0．05），瑞舒伐他汀组和卡托普利组各项指标比较差异无统计学意义（P〉0．05）。结论：瑞舒伐他汀能有效减轻心肌肥厚后心肌组织的纤维化程度，这一效应可能与其降低心肌中高表达的MMP-2、MMP-9有关。

Effect of rosuvastatin on protein expression of matrix metalloproteinase-2 and 9 in rat cardiac hypertrophy model

Objective： To explore the effects of rosuvastatin on protein expression of matrix metalloproteinase- 2 and 9 （ MMP-2, MMP-9） in rat cardiac hypertrophy model. Methods： Fourty SD rats were randomly divided into 4 groups, including control group, Isoprenaline （ISO） group, Captoril （Cap） group and Rosuvastatin （Ros） group, with 10 rats in each group. Cardiac hypertrophy models were induced by injection of ISO into rats of ISO group, Cap group and Ros group, while physiological saline were injected into control group. Then, Ros group were given Ros （4 mg/kg） by intragastric administration per day, Cap group were given Cap 60 mg/kg intragastric administration per day. Body weight （ BW）, heart - weight （HW） and left ventricular weight （LVW） were measured, and their ratios （ HW/BW, LVW/BW） were calculated. The collagen in myocardium of left ventricle were detected. The protein expression of MMP-2 and MMP-9 were examined by immunohistochemieal analysis. Results： ISO induced hypertrophy and extracellular matrix remodeling was shown to locate predominantly in left ventricle, and the protein expression of MMP-2, MMP-9 were increased in this model （P 〈 0. 05）. After Ros treatment, the total amount of collage and protein expression of MMP-2 and MMP-9 were decreased （P 〈 0. 05 ）. The effect of Ros was similar to that of Cap （P 〉 0. 05 ）. Conclusion： Rosuvastatin can relieve the degree of myocardial fibering after cardiac hypertrophy, which was associated with the attenuated expression of myocardial MMP-2 and MMP-9.