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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。
Objective To investigate the effect of fluoxetine on the expression of bone morphogenetic protein receptor 2 (BMPR2) and its preventive effect on pulmonary arterial hypertension (PAH) induced by monocrotaline (MCT) in rats . Methods Twenty-four Wistar rats were randomly divided into three groups: control group, MCT group and fluoxetine-treated group. The hemodynamic indexes were measured with a multi-channel physiological recorder. The morphology of the pulmonary artery was observed by HE staining. The expression of BMPR2 in the pulmonary artery was detected by RT-PCR. Results Compared with the control group, the pulmonary arterial pressure, percentage of pulmonary arterial thickness and right ventricular hypertrophy index in MCT group were significantly increased, while the expression of BMPR2 in pulmonary artery was significantly decreased (P <0.01). After treatment with fluoxetine, fluoxetine significantly inhibited the increase of pulmonary arterial pressure, pulmonary artery remodeling and right ventricular hypertrophy induced by MCT, and reversed the expression of BMPR2 (P <0.05). Conclusions The reconstruction of pulmonary artery may be related to the decreased expression of BMPR2. Fluoxetine may effectively prevent MCT-induced PAH by reversing BMPR2 expression.