4.6

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2.2

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  • ISSN 1674-8301
  • CN 32-1810/R
Hanhua Gao, Can Chen, Shi'an Huang, Bo Li. Quercetin attenuates the progression of monocrotaline-induced pulmonary hypertension in rats[J]. The Journal of Biomedical Research, 2012, 26(2): 98-102. DOI: 10.1016/S1674-8301(12)60018-9
Citation: Hanhua Gao, Can Chen, Shi'an Huang, Bo Li. Quercetin attenuates the progression of monocrotaline-induced pulmonary hypertension in rats[J]. The Journal of Biomedical Research, 2012, 26(2): 98-102. DOI: 10.1016/S1674-8301(12)60018-9

Quercetin attenuates the progression of monocrotaline-induced pulmonary hypertension in rats

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  • Received Date: October 10, 2011
  • 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 pharmacologi -cal effects including improvement of endothelial cell function. However, its pharmacological effects on pul -monary 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, com -pared 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 con -trols ( 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.
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