Effects of baicalin on collagen Ι and collagen ΙΙΙ expression in pulmonary arteries of rats with hypoxic pulmonary hypertension

Liu,Panpan; Yan,Shuangquan; Chen,Mayun; Chen,Ali; Yao,Dan; Xu,Xiaomei; Cai,Xueding; Wang,Liangxing; Huang,Xiaoying

doi:10.3892/ijmm.2015.2110

Effects of baicalin on collagen Ι and collagen ΙΙΙ expression in pulmonary arteries of rats with hypoxic pulmonary hypertension

Authors:
- Panpan Liu
- Shuangquan Yan
- Mayun Chen
- Ali Chen
- Dan Yao
- Xiaomei Xu
- Xueding Cai
- Liangxing Wang
- Xiaoying Huang
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Affiliations: Intensive Care Unit, Ningbo Medical Treatment Center Lihuili Hospital, Ningbo, Zhejiang 315040, P.R. China, Division of Respiratory Medicine, Taizhou Enze Medical Center Luqiao Hospital, Taizhou, Zhejiang 318050, P.R. China, Division of Pulmonary Medicine, The First Affiliated Hospital of Wenzhou Medical University and Key Laboratory of Heart and Lung, Wenzhou, Zhejiang 325035, P.R. China
Published online on: February 25, 2015 https://doi.org/10.3892/ijmm.2015.2110
Pages: 901-908
Copyright: © Liu et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 3.0].

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Abstract

The synthesis and accumulation of collagen play an important role in the formation and progression of hypoxic pulmonary hypertension. Baicalin has been reported to prevent bleomycin-induced pulmonary fibrosis. However, the role of baicalin in the treatment of pulmonary hypertension remains unknown. A disintegrin and metalloprotease with thrombospondin type-1 motif (ADAMTS-1) is a secreted enzyme that acts on a wide variety of extracellular matrix (ECM) substrates associated with vascular diseases. In this study, we aimed to investigate the effects of baicalin on the synthesis of collagen I in rats with pulmonary hypertension induced by hypoxia and the changes in ADAMTS-1 expression. A total of 24 Sprague Dawley rats were randomly assigned to 3 groups as follows: the control group (C), the hypoxia group (H) and the hypoxia + baicalin group (B). The rats in groups H and B were kept in a normobaric hypoxic chamber for 4 weeks, and the rats in group C were exposed to room air. We measured the hemodynamic indexes, including mean pulmonary artery pressure (mPAP), mean systemic (carotid) artery pressure (mSAP), and then calculated the mass ratio of right ventricle to left ventricle plus septum [RV/(LV + S)] to reflect the extent of right ventricular hypertrophy. We measured the mRNA and protein expression levels of type I collagen, type III collagen and ADAMTS-1 by hybridization in situ, and immunohistochemistry and western blot analysis, respectively. The results revealed that treatment with baicalin significantly reduced pulmonary artery pressure and attenuated the remodeling of the pulmonary artery under hypoxic conditions by increasing the expression of ADAMTS-1, so that the synthesis of type I collagen and its mRNA expression were inhibited. In conclusion, baicalin effectively inhibits the synthesis of collagen I in pulmonary arteries and this is associated with an increase in the expression of ADAMTS-1. Thus, treatment with baicalin may be an effective method for lowering pulmonary artery pressure and preventing pulmonary artery remodeling.

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