辛伐他汀对野百合碱诱导的肺动脉高压大鼠IL-6和IL-8表达的影响

目的观察辛伐他汀对野百合碱（MCT）诱导的肺动脉高压大鼠炎症细胞因子IL-6和IL-8表达的影响,探讨辛伐他汀作用于肺动脉高压的机制。方法将30只健康雄性SD大鼠随机平均分为正常对照组、MCT诱导的肺动脉高压组（模型对照组）、辛伐他汀干预治疗组（治疗组）。模型对照组和治疗组注射野百合碱造模。治疗21 d后,采用右心导管法检测大鼠平均肺动脉压（mPAP）;称量RV和LV＋S,计算右心肥大指数（RVHI）。采用RT-PCR检测大鼠肺组织中IL-6和IL-8 mRNA的表达,采用ELISA法检测大鼠血清中IL-6和IL-8水平。结果模型对照组mPAP和RVHI值显著高于治疗组和正常对照组,治疗组和正常对照组mPAP和RVHI值比较无显著性差异。模型对照组大鼠肺组织中IL-6和IL-8 mRNA的表达和血清中IL-6和IL-8水平显著高于正常对照组和治疗组,而治疗组大鼠肺组织中IL-6和IL-8 mRNA的表达和血清中IL-6水平与正常对照组比较无显著性差异,但治疗组大鼠血清IL-8水平高于正常对照组（P〈0.05）。结论辛伐他汀可通过抑制MCT诱导大鼠肺动脉高压模型大鼠肺组织中炎性细胞因子的表达、下调大鼠炎性细胞因子的分泌,达到对肺动脉高压的治疗作用。

Effect of simvastatin on expression of IL-6 and IL-8 in monocrotaline-induced pulmonary hypertension in rats

Objective To study the effect of simvastatin on the expression of inflammatory cytokines IL-6 and IL-8 in monocrotaline (MCT)-induced pulmonary hypertension in rats, and to investigate the therapeutic mechanism of simvas-tatin for pulmonary hypertension. Methods Thirty SD rats were divided into 3 groups:a normal control group,an MCT-induced pulmonary hypertension group (model control group),and a simvastatin treatment group (therapeutic group). The rats in the model control group and the therapeutic group were injected MCT to induce pulmonary hypertension. After 21 days, the mean pulmonary arterial pressure (mPAP) and right venirieular hypertophy index (RVHI) were measured, and the expression of IL-6 and IL-8 mRNA in the lung tissue and the levels of IL-6 and IL-8 were detected.Results mPAP and RVHI and the expression of IL-6 and IL-8 mRNA in the lung tissue and the levels of IL-6 and IL-8 in the serum in the model control group were higher than those in the normal control group and the therapeutic group, moreover there were no difference of mPAP and RVHI, and mRNA expression of IL-6 and IL-8 in the tissues and levels of IL-6 in the serum between the thrapeutic group and the normal control group.The level of IL-8 in the therapeutic group was higher than that in the normal group.Conclusion Simvastatin has therapeutic effect on pulmonary hypertension through down-regulating IL-6 and IL-8 expression.