Resveratrol Attenuates Monocrotaline-Induced Pulmonary Hypertension in Rats
نویسندگان
چکیده
Background and Objectives:Resveratrol (RVT) is a polyphenolic phytoalexin, and it has been demonstrated to be capable of protecting against cardiovascular disease. The aim of this study was to identify whether RVT might protect against monocrotaline (MCT)-induced pulmonary hypertension and whether vascular endothelial growth factor (VEGF), endothelial nitric oxide synthase (eNOS), and inducible nitric oxide synthase (iNOS) are involved in the beneficial effects. Materials and Methods:Thirty Sprague Dawley rats were divided into three groups: the control (n=6), the MCT (n=12) and the MCT with RVT (5 mg/kg/day, n=12) groups. After 28 days, the tissue samples were obtained for morphometric analysis and Western blotting. Results:In the MCT group, the right ventricle/(left ventricle+septum) weight ratio was significantly increased compared with that of the control group (0.51±0.07 vs. 0.20±0.03, p<0.01), which was markedly suppressed in the RVT treated group (0.35± 0.08, p<0.01). Histological analysis also showed that MCT treatment increased the medial wall thickness of the pulmonary arterioles compared with that of the control group (36±8% vs. 17±5%, p<0.01), which also was significantly suppressed in the RVT treated group (27±5%, p<0.01). In addition, Western blot demonstrated the decreased expression of VEGF in the MCT group (p<0.01), which was upregulated after long term RVT treatment (p<0.01). The expression of eNOS was increased after MCT treatment (p<0.01), but upregulation of eNOS could not be reversed by the RVT treatment. The expression of iNOS was not significantly modulated. Conclusion: These results suggest that RVT attenuates MCT-induced pulmonary hypertension and it may represent a new strategy for the treatment of pulmonary hypertension. (Korean Circulation J 2006;36:683-687)
منابع مشابه
Chronic intermittent hypobaric hypoxia attenuates monocrotaline-induced pulmonary arterial hypertension via modulating inflammation and suppressing NF-κB /p38 pathway
Objective(s): Inflammation is involved in various forms of pulmonary arterial hypertension (PAH). Although the pathophysiology of PAH remains uncertain, NF-κB and p38 mitogen-activated protein kinase (p38 MAPK) has been reportedto be associated with many inflammatory mediators of PAH. This study aimed to evaluate the effect of chronic intermittent hypobaric hypoxia (CIHH) on pulmonary inflammat...
متن کاملPulmonary Hypertension Resveratrol Prevents Monocrotaline-Induced Pulmonary Hypertension in Rats
Proliferation of pulmonary arterial smooth muscle cells, endothelial dysfunction, oxidative stress, and inflammation promotes the development of pulmonary hypertension. Resveratrol is a polyphenolic compound that exerts antioxidant and anti-inflammatory protective effects in the systemic circulation, but its effects on pulmonary arteries remain poorly defined. The present study was undertaken t...
متن کاملResveratrol prevents monocrotaline-induced pulmonary hypertension in rats.
Proliferation of pulmonary arterial smooth muscle cells, endothelial dysfunction, oxidative stress, and inflammation promotes the development of pulmonary hypertension. Resveratrol is a polyphenolic compound that exerts antioxidant and anti-inflammatory protective effects in the systemic circulation, but its effects on pulmonary arteries remain poorly defined. The present study was undertaken t...
متن کاملCalorie Restriction Attenuates Monocrotaline-induced Pulmonary Arterial Hypertension in Rats: Erratum
متن کامل
Longitudinal In Vivo SPECT/CT Imaging Reveals Morphological Changes and Cardiopulmonary Apoptosis in a Rodent Model of Pulmonary Arterial Hypertension
Pulmonary arterial hypertension (PAH) has a complex pathogenesis involving both heart and lungs. Animal models can reflect aspects of the human pathology and provide insights into the development and underlying mechanisms of disease. Because of the variability of most animal models of PAH, serial in vivo measurements of cardiopulmonary function, morphology, and markers of pathology can enhance ...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
دوره شماره
صفحات -
تاریخ انتشار 2006