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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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Effect of baicalin on hypoxia-induced pulmonary hypertension. (A) Demonstrative traces of mean pulmonary artery pressure (mPAP) in each group of animals. (B) mPAP. *P<0.01, compared with hypoxia group; #P<0.01, compared with hypoxia group. (C) Mean systemic (carotid) arterial pressure (mSAP).
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f1-ijmm-35-04-0901: Effect of baicalin on hypoxia-induced pulmonary hypertension. (A) Demonstrative traces of mean pulmonary artery pressure (mPAP) in each group of animals. (B) mPAP. *P<0.01, compared with hypoxia group; #P<0.01, compared with hypoxia group. (C) Mean systemic (carotid) arterial pressure (mSAP).

Mentions: We measured mPAP and mSAP to reflect the hemodynamic changes. Hematoxylin and eosin (H&E) staining of the pulmonary artery tissue was carried out to calculate the ratio of the pulmonary artery wall thickness to the total area of the artery (WA/TA) for a comparison of the thickening of the arteries among the 3 groups. The RV/(LV + S) was calculated to reflect the extent of right ventricular hypertrophy. mPAP increased from 16.3±2.7 to 23.6±0.9 mmHg following the induction of chronic hypoxia (P<0.01), and treatment with baicalin effectively attenuated this increase, decreasing mPAP to 17.0±2.7 mmHg (P<0.01; Fig. 1A and B). However, there was no statistically significant difference in mSAP among the 3 groups (Fig. 1C). The thickness of the arteries which was induced by chronic hypoxia (77.75±6.79%) was much more obvious than that of the rats in group C (61.00±6.86%) (P<0.01). Bacalin markedly attenuated this effect, decreasing the WA/TA and the WA/TA% to 67.72±6.76% (P<0.01; Fig. 2A and B). The RV/(LV + S)% was markedly elevated in the rats in group H (34.18±2.43%) compared with the rats in group C (26.57±0.77%) (P<0.01). Following the injection of bacalin, the RV/(LV + S)% decreased to 31.36±2.70% and right ventricular hypertrophy was significantly attenuated (P<0.05; Fig. 2C).


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)

Effect of baicalin on hypoxia-induced pulmonary hypertension. (A) Demonstrative traces of mean pulmonary artery pressure (mPAP) in each group of animals. (B) mPAP. *P<0.01, compared with hypoxia group; #P<0.01, compared with hypoxia group. (C) Mean systemic (carotid) arterial pressure (mSAP).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f1-ijmm-35-04-0901: Effect of baicalin on hypoxia-induced pulmonary hypertension. (A) Demonstrative traces of mean pulmonary artery pressure (mPAP) in each group of animals. (B) mPAP. *P<0.01, compared with hypoxia group; #P<0.01, compared with hypoxia group. (C) Mean systemic (carotid) arterial pressure (mSAP).
Mentions: We measured mPAP and mSAP to reflect the hemodynamic changes. Hematoxylin and eosin (H&E) staining of the pulmonary artery tissue was carried out to calculate the ratio of the pulmonary artery wall thickness to the total area of the artery (WA/TA) for a comparison of the thickening of the arteries among the 3 groups. The RV/(LV + S) was calculated to reflect the extent of right ventricular hypertrophy. mPAP increased from 16.3±2.7 to 23.6±0.9 mmHg following the induction of chronic hypoxia (P<0.01), and treatment with baicalin effectively attenuated this increase, decreasing mPAP to 17.0±2.7 mmHg (P<0.01; Fig. 1A and B). However, there was no statistically significant difference in mSAP among the 3 groups (Fig. 1C). The thickness of the arteries which was induced by chronic hypoxia (77.75±6.79%) was much more obvious than that of the rats in group C (61.00±6.86%) (P<0.01). Bacalin markedly attenuated this effect, decreasing the WA/TA and the WA/TA% to 67.72±6.76% (P<0.01; Fig. 2A and B). The RV/(LV + S)% was markedly elevated in the rats in group H (34.18±2.43%) compared with the rats in group C (26.57±0.77%) (P<0.01). Following the injection of bacalin, the RV/(LV + S)% decreased to 31.36±2.70% and right ventricular hypertrophy was significantly attenuated (P<0.05; Fig. 2C).

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