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Int. J. Mol. Sci. 2014, 15(5), 8153-8168; doi:10.3390/ijms15058153

Baicalin Inhibits Hypoxia-Induced Pulmonary Artery Smooth Muscle Cell Proliferation via the AKT/HIF-1α/p27-Associated Pathway

1
Department of Respiratory Medicine, the First Affiliated Hospital of Dalian Medical University, No. 222 Zhongshan Road, Dalian 116000, China
2
Department of Clinical Medicine, Yijishan Hospital of Wannan Medical College, Wuhu 241001, China
3
Department of Oncology, Dalian University Affiliated Xinhua Hospital, No. 156 Wansui Street, Dalian 116000, China
4
Department of Gastroenterology, the First Affiliated Hospital of Dalian Medical University, No. 222 Zhongshan Road, Dalian 116000, China
5
School of Public Health, Dalian Medical University, 9 Western Lvshun South Road, Dalian 116000, China
6
Department of Cardiology, the First Affiliated Hospital of Dalian Medical University, No. 222 Zhongshan Road, Dalian 116000, China
These authors contributed equally to this work.
*
Author to whom correspondence should be addressed.
Received: 25 March 2014 / Revised: 27 April 2014 / Accepted: 30 April 2014 / Published: 9 May 2014
(This article belongs to the Section Biochemistry, Molecular and Cellular Biology)
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Abstract

Baicalin, a flavonoid compound purified from the dry roots of Scutellaria baicalensis Georgi, has been shown to possess various pharmacological actions. Previous studies have revealed that baicalin inhibits the growth of cancer cells through the induction of apoptosis. Pulmonary arterial hypertension (PAH) is a devastating disease characterized by enhanced pulmonary artery smooth muscle cell (PASMCs) proliferation and suppressed apoptosis. However, the potential mechanism of baicalin in the regulation of PASMC proliferation and the prevention of cardiovascular diseases remains unexplored. To test the effects of baicalin on hypoxia, we used rats treated with or without baicalin (100 mg·kg−1 each rat) at the beginning of the third week after hypoxia. Hemodynamic and pulmonary pathomorphology data showed that right ventricular systolic pressures (RVSP), the weight of the right ventricle/left ventricle plus septum (RV/LV + S) ratio and the medial width of pulmonary arterioles were much higher in chronic hypoxia. However, baicalin treatment repressed the elevation of RVSP, RV/LV + S and attenuated the pulmonary vascular structure remodeling (PVSR) of pulmonary arterioles induced by chronic hypoxia. Additionally, baicalin (10 and 20 μmol·L−1) treatment suppressed the proliferation of PASMCs and attenuated the expression of hypoxia-inducible factor-α (HIF-α) under hypoxia exposure. Meanwhile, baicalin reversed the hypoxia-induced reduction of p27 and increased AKT/protein kinase B phosphorylation p-AKT both in vivo and in vitro. These results suggested that baicalin could effectively attenuate PVSR and hypoxic pulmonary hypertension. View Full-Text
Keywords: baicalin; pulmonary hypertension; pulmonary artery smooth muscle cells; proliferation baicalin; pulmonary hypertension; pulmonary artery smooth muscle cells; proliferation
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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MDPI and ACS Style

Zhang, L.; Pu, Z.; Wang, J.; Zhang, Z.; Hu, D.; Wang, J. Baicalin Inhibits Hypoxia-Induced Pulmonary Artery Smooth Muscle Cell Proliferation via the AKT/HIF-1α/p27-Associated Pathway. Int. J. Mol. Sci. 2014, 15, 8153-8168.

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