Intermedin inhibits pulmonary collagen synthesis in rats with pulmonary hypertension induced by high pulmonary blood flow
10.3969/j.issn.1000-4718.2014.12.012
- VernacularTitle:中介素抑制高肺血流性肺动脉高压大鼠肺组织胶原生成
- Author:
Lulu PANG
;
Jianguang QI
;
Yang GAO
;
Hongfang JIN
;
Junbao DU
- Publication Type:Journal Article
- Keywords:
Pulmonary hypertension;
High pulmonary blood flow;
Collagen;
Intermedin
- From:
Chinese Journal of Pathophysiology
2014;(12):2185-2189
- CountryChina
- Language:Chinese
-
Abstract:
[ ABSTRACT] AIM:To explore the regulatory effect of intermedin ( IMD) on pulmonary collagen synthesis and ac-cumulation in rats with pulmonary hypertension induced by high pulmonary blood flow.METHODS: Healthy male SD rats (n=20) were randomly divided into control group (n=7), shunt group (n=7) and shunt with IMD group (n=6).The shunting of abdominal aorta and inferior vena cava was produced in rats of shunt group and shunt with IMD group.After 8 weeks, IMD was administered into the rats of shunt with IMD group subcutaneously by mini-osmotic pump for 2 weeks.Mean pulmonary artery pressure (mPAP), relative medial thickness (RMT) of pulmonary arteries, contents of hydroxyproline, collagen type I and III, bone morphogenetic protein-2 (BMP-2), and the mRNA expression of procollagen I and III in lung tissues were measured and compared.RESULTS:Compared with control group, mPAP and RMT of medium and small pul-monary arteries in the rats of shunt group were significantly increased.Meanwhile, the lung hydroxyproline, collagens I and III and BMP-2 contents, and the mRNA expression of lung procollagen I and III were all significantly increased compared with control group.However, IMD significantly decreased mPAP, alleviated the changes of pulmonary vascular micro-struc-ture, decreased the collagen accumulation and pulmonary tissue homogenate BMP-2 contents, and inhibited the mRNA ex-pression of procollagen I and III in the lung tissue of shunting rats.CONCLUSION:IMD plays a protective role in the de-velopment of pulmonary hypertension and pulmonary vascular structural remodeling induced by high blood flow by inhibiting pulmonary collagen synthesis and accumulation, possibly in association with the BMP-2 pathway.
