Effect of fluoxetine on monocrotaline-induced remodeling of pulmonary arteries and right ventricle in rats
Huailiang Wang
Abstract
Huailiang Wang
Abstract
Objective To investigate the effect of fluoxetine on monocrotaline (MCT)-induced remodeling of the pulmonary arteries and the right ventricle in rats. Methods Models of pulmonary arterial hypertension (PAH) were established by MCT. 40 Wistar rats were divided into four groups: control group, model group (MCT), treatment group with fluoxetine at 2mg/kg (MCT+F2) and at 10mg/kg (MCT+F10) respectively. Pulmonary arterial pressure and systemic arterial pressure were recorded by the polygraph system. The lung and heart sections were stained with hematoxyline-eosine (HE), followed by measurement of the percentage of medial wall thickness and right ventricular index. The protein expression of matrix metalloproteinases 9 (MMP9) in right ventricle was detected by western blotting. Results Compared with the control group, MCT caused pulmonary arterial hypertension, pulmonary arterial remodeling, right ventricular hypertrophy, myocardial injury and significantly increased expression of MMP9 in the right ventricle. Compared with the MCT group, fluoxetine dose-dependently decreased the above indexes, and the inhibitory effect was markedly in MCT+F10 group ( P 0.05). Conclusion Fluoxetine effectively attenuated the remodeling of pulmonary arteries and right ventricle in rats.
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Objective To investigate the effect of fluoxetine on monocrotaline (MCT)-induced remodeling of the pulmonary arteries and the right ventricle in rats. Methods Models of pulmonary arterial hypertension (PAH) were established by MCT. 40 Wistar rats were divided into four groups: control group, model group (MCT), treatment group with fluoxetine at 2mg/kg (MCT+F2) and at 10mg/kg (MCT+F10) respectively. Pulmonary arterial pressure and systemic arterial pressure were recorded by the polygraph system. The lung and heart sections were stained with hematoxyline-eosine (HE), followed by measurement of the percentage of medial wall thickness and right ventricular index. The protein expression of matrix metalloproteinases 9 (MMP9) in right ventricle was detected by western blotting. Results Compared with the control group, MCT caused pulmonary arterial hypertension, pulmonary arterial remodeling, right ventricular hypertrophy, myocardial injury and significantly increased expression of MMP9 in the right ventricle. Compared with the MCT group, fluoxetine dose-dependently decreased the above indexes, and the inhibitory effect was markedly in MCT+F10 group ( P 0.05). Conclusion Fluoxetine effectively attenuated the remodeling of pulmonary arteries and right ventricle in rats.
Key concepts: Ventricle, Right ventricular hypertrophy, Internal medicine, Pulmonary artery, Medicine, Cardiology, Pulmonary hypertension, Lung