Fluoxetine influences the expression of BMPR2 and prevents monocrotaline-induced pulmonary arterial hypertension in rats
Huailiang Wang
Abstract
Huailiang Wang
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.
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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.
Key concepts: BMPR2, Ventricle, Pulmonary hypertension, Fluoxetine, Internal medicine, Right ventricular hypertrophy, Pulmonary artery, Medicine