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首页> 外文期刊>Korean Circulation Journal >Changes of Pulmonary Pathology and Gene Expressions After Simvastatin Treatment in the Monocrotaline-Induced Pulmonary Hypertension Rat Model
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Changes of Pulmonary Pathology and Gene Expressions After Simvastatin Treatment in the Monocrotaline-Induced Pulmonary Hypertension Rat Model

机译：辛伐他汀引起的吗啉他汀诱导的肺动脉高压大鼠模型中肺病理学和基因表达的变化

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Background and Objectives Simvastatin's properties are suggestive of a potential pathophysiologic role in pulmonary hypertension. The objectives of this study were to investigate changes of pulmonary pathology and gene expressions, including endothelin (ET)-1, endothelin receptor A (ERA), inducible nitric oxide synthase (NOS2), endothelial nitric oxide synthase (NOS3), matrix metalloproteinase (MMP) 2, tissue inhibitor of matrix metalloproteinases (TIMP) and caspase 3, and to evaluate the effect of simvastatin on monocrotaline (M)-induced pulmonary hypertension. Materials and Methods Six week old male Sprague-Dawley rats were treated, as follows: control group, subcutaneous (sc) injection of saline; M group, sc injection of M (60 mg/kg); and simvastatin group, sc injection of M (60 mg/kg) plus 10 mg/kg/day simvastatin orally. Results On day 28, right ventricular hypertrophy (RVH) significantly decreased in the simvastatin group compared to the M group. Similarly, right ventricular pressure significantly decreased in the simvastatin group on day 28. From day 7, the ratio of medial thickening of the pulmonary artery was significantly increased in the M group, but there was no significant change in the simvastatin group. The number of muscular pulmonary arterioles was significantly reduced in the simvastatin group. On day 5, gene expressions of ET-1, ERA, NOS2, NOS3, MMP and TIMP significantly decreased in the simvastatin group. Conclusion Administration of simvastatin exerted weak inhibitory effects on RVH and on the number of muscular pulmonary arterioles, during the development of M-induced pulmonary hypertension in rats. Simvastatin decreased gene expressions on day 5.
机译：背景和目的辛伐他汀的性质提示在肺动脉高压中潜在的病理生理作用。这项研究的目的是调查肺病理和基因表达的变化，包括内皮素（ET）-1，内皮素受体A（ERA），诱导型一氧化氮合酶（NOS2），内皮型一氧化氮合酶（NOS3），基质金属蛋白酶（ MMP）2，基质金属蛋白酶（TIMP）和半胱天冬酶3的组织抑制剂，并评估辛伐他汀对单芥子碱（M）诱导的肺动脉高压的作用。材料和方法六周大的Sprague-Dawley雄性大鼠的治疗方法如下：对照组，皮下注射生理盐水;皮下注射生理盐水。 M组，皮下注射M（60 mg / kg）;辛伐他汀组，皮下注射M（60 mg / kg）加10 mg / kg / day辛伐他汀口服。结果在第28天，辛伐他汀组的右心室肥大（RVH）较M组明显降低。同样，在第28天，辛伐他汀组右心室压力显着降低。从第7天起，M组肺动脉内侧增厚的比率显着增加，但在辛伐他汀组中无明显变化。辛伐他汀组肌肉肺小动脉数量明显减少。在第5天，辛伐他汀组中ET-1，ERA，NOS2，NOS3，MMP和TIMP的基因表达显着降低。结论辛伐他汀的给药在M诱发的大鼠肺动脉高压发展过程中对RVH和肌肉肺小动脉数量具有微弱的抑制作用。辛伐他汀在第5天降低了基因表达。

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