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

Liu P, Yan S, Chen M, Chen A, Yao D, Xu X, Cai X, Wang L, Huang X - Int. J. Mol. Med. (2015)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Intensive Care Unit, Ningbo Medical Treatment Center Lihuili Hospital, Ningbo, Zhejiang 315040, P.R. China.

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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Protein expression of collagen I and III in pulmonary arterioles (by immunohistochemical analysis). (A) Expression of collagen I and III in pulmonary arterioles (scale bar, 50 μm; magnification, x400). (B) Expression of collagen I in pulmonary arterioles. *P<0.01, compared with hypoxia group; #P<0.05, compared with hypoxia group. (C) Expression of collagen III in pulmonary arterioles.
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f3-ijmm-35-04-0901: Protein expression of collagen I and III in pulmonary arterioles (by immunohistochemical analysis). (A) Expression of collagen I and III in pulmonary arterioles (scale bar, 50 μm; magnification, x400). (B) Expression of collagen I in pulmonary arterioles. *P<0.01, compared with hypoxia group; #P<0.05, compared with hypoxia group. (C) Expression of collagen III in pulmonary arterioles.

Mentions: Under the condition of chronic hypoxia, the OD value of collagen I noticeably increased compared with the normal condition in group C (0.242±0.043 vs. 0.188±0.021, P<0.01), and its mRNA expression increased from 0.195±0.014 in group C to 0.220±0.033 in group H (Figs. 3 and 4). However, as expected, treatment with baicalin decreased the OD value and mRNA expression of collagen I to 0.201±0.019 (P<0.05) and 0.196±0.018 (P<0.05), respectively (Figs. 3 and 4). Western blot analysis also revealed that chronic hypoxia markedly upregulated the protein expression of collagen I from 0.175±0.119 to 0.417±0.305 (P<0.05), and treatment with baicalin markedly decreased this expression (0.188±0.183; P<0.05; Fig. 5).


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

Liu P, Yan S, Chen M, Chen A, Yao D, Xu X, Cai X, Wang L, Huang X - Int. J. Mol. Med. (2015)

Protein expression of collagen I and III in pulmonary arterioles (by immunohistochemical analysis). (A) Expression of collagen I and III in pulmonary arterioles (scale bar, 50 μm; magnification, x400). (B) Expression of collagen I in pulmonary arterioles. *P<0.01, compared with hypoxia group; #P<0.05, compared with hypoxia group. (C) Expression of collagen III in pulmonary arterioles.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4356435&req=5

f3-ijmm-35-04-0901: Protein expression of collagen I and III in pulmonary arterioles (by immunohistochemical analysis). (A) Expression of collagen I and III in pulmonary arterioles (scale bar, 50 μm; magnification, x400). (B) Expression of collagen I in pulmonary arterioles. *P<0.01, compared with hypoxia group; #P<0.05, compared with hypoxia group. (C) Expression of collagen III in pulmonary arterioles.
Mentions: Under the condition of chronic hypoxia, the OD value of collagen I noticeably increased compared with the normal condition in group C (0.242±0.043 vs. 0.188±0.021, P<0.01), and its mRNA expression increased from 0.195±0.014 in group C to 0.220±0.033 in group H (Figs. 3 and 4). However, as expected, treatment with baicalin decreased the OD value and mRNA expression of collagen I to 0.201±0.019 (P<0.05) and 0.196±0.018 (P<0.05), respectively (Figs. 3 and 4). Western blot analysis also revealed that chronic hypoxia markedly upregulated the protein expression of collagen I from 0.175±0.119 to 0.417±0.305 (P<0.05), and treatment with baicalin markedly decreased this expression (0.188±0.183; P<0.05; Fig. 5).

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Intensive Care Unit, Ningbo Medical Treatment Center Lihuili Hospital, Ningbo, Zhejiang 315040, P.R. China.

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.

Show MeSH
Related in: MedlinePlus