Abstract
Pulmonary arterial hypertension (PAH) is a progressive disease associated with increased constriction and remodeling of the pulmonary vasculature. Quercetin is a natural flavonoid and has a variety of pharmacological effects including improvement of endothelial cell function. However, its pharmacological effects on pulmonary hypertension have been rarely reported. We sought to observe the protective effect of quercetin in rats with monocrotaline induced PAH. We divided 30 male Sprague-Dawley rats randomly into three groups with ten rats in each group: the monocrotaline group, the quercetin group and the control group. We found that, compared with the controls, the mean pulmonary artery pressure (mPAP) and the right ventricular hypertrophy index in the monocrotaline group were significantly higher (P < 0.01). Quercetin caused a significant reduction both in the mPAP and right ventricular hypertrophy index compared with the monocrotaline group (P < 0.01) while no difference was found between the quercetin group and the control group (P > 0.05). Monocrotaline induced a marked increase in the wall thickness (WT) in small and mid-sized pulmonary arteries compared with the controls (P < 0.01). Monocrotaline also induced a marked increase in the wall area (WA) in small [(56.38±6.65)% in monocrotaline vs. (19.80±4.63)% in control] and mid-sized [(43.71±5.38)% in monocrotaline vs. (14.24±3.66)% in control] pulmonary arteries (P < 0.01). Quercetin treatment markedly reduced monocrotaline induced increase in both WT and WA (P < 0.01), which, however, still remained significantly elevated compared with those of the controls (P < 0.01). Furthermore, compared with controls, proliferating cell nuclear antigen (PCNA) expression in the pulmonary artery tissues was markedly increased by monocrotaline [(45.59±1.27) in monocrotaline vs. (9.64±0.69) in controls], which was significantly attenuated by quercetin. Our animal experiment indicated that quercetin could have protective effects on monocrotaline-induced PAH.
Highlights
Pulmonary arterial hypertension (PAH) is a progressive disease associated with increased constriction and remodeling of the pulmonary vasculature, leading to right heart failure with a mean survival time typically less than 3 years
With quercetin caused a significant reduction both in the mean pulmonary artery pressure (mPAP) and right ventricular hypertrophy index compared with the monocrotaline group (P < 0.01), while no difference was found between the quercetin group and the control group (P > 0.05)
We established monocrotaline-induced rat PAH model and measurement of the mPAP showed that compared with the controls, the mPAP in the monocrotaline group was significantly higher (P < 0.01), suggesting that the PAH model was successfully established
Summary
Pulmonary arterial hypertension (PAH) is a progressive disease associated with increased constriction and remodeling of the pulmonary vasculature, leading to right heart failure with a mean survival time typically less than 3 years. PAH can be diagnosed by measurement of the mean pulmonary artery pressure (mPAP) via right heart catheterization. The current lack of knowledge about PAH and effective diagnostic methods for PAH leads to treatment delays and poor prognosis, and patients succumb to right heart failure. Monocrotaline is a poisonous crystalline alkaloid C16H23NO6 in a leguminous plant of the genus Crotalaria (C. spectabilis) and in the same genus of other plants. It is metabolized into monocrotaline pyrrole in the rat liver[1].
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