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目的:探讨3-羟基-3-甲基戊二酰辅酶A还原酶(HMG-COA)抑制剂辛伐他汀对肺动脉高压(PAH)大鼠环氧合酶(COX-2)的影响。方法:雄性SD大鼠30只,随机分为正常对照组、PAH模型组和辛伐他汀干预组,每组10只。用PM-8000型多参数监护仪及Elastin Van Gieson染色法,分别测定各组大鼠的平均肺动脉压力及肺小动脉新生内膜增殖度和平均血管阻塞计分(VOS)的改变。用免疫组化染色法和荧光定量PCR法,测定肺组织中的COX-2在蛋白和基因的水平上表达的差异。结果:PAH模型组大鼠的平均肺动脉压力、肺小动脉新生内膜增殖度和VOS的改变,均较正常对照组显著增加(P<0.05),其COX-2在蛋白和基因的水平上的表达都明显高于正常对照组(P<0.05)。辛伐他汀干预后,大鼠的平均肺动脉压力、肺小动脉新生内膜增殖度和VOS,均较PAH模型组显著减少(P<0.05),COX-2在蛋白和基因的水平上的表达都明显低于PAH模型组(P<0.05)。结论:辛伐他汀可抑制肺动脉内COX-2的表达来抑制PAH形成。
Objective: To investigate the effect of simvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-COA) inhibitor, on cyclooxygenase (COX-2) in pulmonary hypertension (PAH) rats. Methods: Thirty male SD rats were randomly divided into normal control group, PAH model group and simvastatin intervention group, with 10 rats in each group. The changes of mean pulmonary arterial pressure, neointimal hyperplasia and mean vascular occlusion score (VOS) of rats in each group were measured by PM-8000 multi-parameter monitor and Elastin Van Gieson staining. The expression of COX-2 in lung tissue at protein and gene level was determined by immunohistochemistry and fluorescence quantitative PCR. Results: The mean pulmonary arterial pressure, neointimal hyperplasia and VOS of pulmonary arterioles in PAH model group were significantly higher than those in normal control group (P <0.05). The COX-2 protein and gene level The expression was significantly higher than the normal control group (P <0.05). Compared with PAH model group, the mean pulmonary arterial pressure, pulmonary arteriolar neointimal hyperplasia and VOS in rats after simvastatin intervention were significantly decreased (P <0.05). The expression of COX-2 at protein and gene level Significantly lower than the PAH model group (P <0.05). Conclusion: Simvastatin can inhibit the expression of COX-2 in the pulmonary artery to inhibit the formation of PAH.