【摘要】 目的探讨氟西汀对骨形态生成蛋白受体2(bone morphogenetic protein receptor 2,BMPR2)表达的影响以及对野百合碱(monocrotaline,MCT)诱导大鼠肺动脉高压(pulmonary arterial hypertension,PAH)的预防作用。方法将24只Wistar大鼠随机分成三组:对照组、MCT组和氟西汀处理组。采用多导生理记录仪测量血流动力学相关指标,HE染色方法观察肺动脉的形态学改变,以及利用RT-PCR方法检测肺动脉BMPR2的表达。结果与对照组相比,MCT组肺动脉压力、肺动脉中膜厚度百分比以及右心肥厚指数均明显升高,BMPR2在肺动脉上的表达明显减少(<0.01)。给予氟西汀处理后,氟西汀明显抑制了MCT诱发的肺动脉压力的升高、肺动脉重构和右心肥厚,并逆转了BMPR2的表达(<0.05)。结论肺动脉的构型重建可能与BMPR2的表达减少有关。氟西汀可能通过逆转BMPR2的表达有效地预防MCT诱导的PAH。更多还原

【Abstract】 Objective To investigate the influence of fluoxetine on bone morphogenetic protein receptor 2(BMPR2) expression in the pulmonary arteries and the preventive effect of fluoxetine on monocrotaline(MCT)-induced pulmonary arterial hypertension(PAH) in rats.Methods Twenty-four Wistar rats were randomly divided into 3 groups: control group,MCT group and fluoxetine-treated group.The hemodynamic measurements were recorded by Polygraph System.Morphological changes of the pulmonary arteries were observed by hematoxyline-eosine(HE).BMPR2 mRNA levels in the pulmonary arteries were detected by RT-PCR.Results Compared with the control group,MCT caused pulmonary arterial hypertension and the significant increases in the medial wall thickness percentage of the pulmonary arteries and right ventricle hypertrophic indexes,and reduced the expression of BMPR2 in the pulmonary arteries(<0.01).After fluoxetine-treatment,the pulmonary arterial remodelling and the right ventricle hypertrophy were markedly inhibited and BMPR2 mRNA level was significantly reversed by fluoxetine(<0.05).Conclusion Pulmonary arterial remodelling was probably associated with the reduction of BMPR2 expression in the pulmonary arteries,prevented PAH by fluoxetine might be related to reversing BMPR2 expression.更多还原