中文摘要：

目的 通过体外心肌细胞培养和在体动物实验方法，观察阿托伐他汀对大鼠心肌肥大的抑制作用，以及对心肌中炎性细胞因子的影响，探讨该类药物影响心肌肥大可能涉及的作用机制。方法 体外原代培养新生大鼠的心肌细胞，以血管紧张素Ⅱ刺激建立心肌肥大模型，给予不同浓度的阿托伐他汀处理。采用RT-PCR法检测脑钠素（BNP）、基质金属蛋白酶9（MMP9）和白细胞介素1β（IL-1β）mRNA的表达，并以^3H-亮氨酸掺入测定心肌细胞蛋白合成速率。在体实验中通过不完全结扎大鼠的腹主动脉，使压力过度负荷增加造成左心室肥厚，以阿托伐他汀治疗4周，RT-PCR检测IL-1β，心调理素-1（CT-1）的表达，并观察心脏的病理学改变。结果心肌细胞肥大模型出现后，心肌细胞的BNP、MMP9和IL-1βmRNA的表达以及蛋白合成速率增加。经不同浓度的阿托伐他汀处理后，这些变化得以减轻。阿托伐他汀抑制压力负荷升高引起的左心室心肌BNP，IL-1β，CT-1的mRNA表达的增加，并减轻大鼠心脏重／体重比值、左心室壁厚度和心肌细胞平均直径的增加。结论 阿托伐他汀可能通过抗炎作用抑制大鼠心肌肥大，对防治以心肌肥厚为特征的心血管疾病可能有一定的应用前景。

英文摘要：

Objective To investigate the effects of atorvastatin on myocardial hypertrophy in vitro and in vivo. Methods Angiotensin I1 was used to establish hypertrophy of cardiac myocytes and atorvastatin at various dosages was applied to these myocytes in vitro. Cytokines and brain natriuretic peptide（BNP） mRNA expression was evaluated by RT-PCR,and the rate of protein synthesis in cardiac myocytes was measured by s H-leucine incorporation. Left ventricular hypertrophy was induced by incomplete ligation of abdominal aorta of rats and atorvastatin （5 mg·kg^-1·d^-1） was administrated one week prior to the operation until 4 weeks after the operation. Cytokine mRNA expression in left ventricle was measured by RT-PCR and left ventricular wall thickness and myocyte diameter were determined by pathological method. Results Atorvastatin inhibited interleukin-1β, matrix metalloproteinase 9 and BNP mRNA expression, as well as ^3H-leucine incorporation in neonatal rat cardiac myocytes induced by angiotensin Ⅱ in a dose-dependent manner in vitro. Furthermore, atorvastatin reduced the mRNA expression of BNP, interleukin-1β and cardiotropin-1, and inhibited the pressure overload-induced increase in the ratio of heart weight to body weight, left ventricular wall thickness and myocyte diameter of rats in vivo. Conclusions Atorvastatin inhibits myocardial hypertrophy of rats in vitro and in vivo, and may have clinical prospect in prevention and treatment of cardiovascular diseases characterized by myocardial hypertrophy.