Effect and mechanism of chimonin on pulmonary hypertention of chronic hypoxia and hypercapnic rats.
- Author:
Xiao-Ying HUANG
1
;
Liang-Xing WANG
;
Ming LI
;
Shao-Xian CHEN
;
Zheng-Jie XU
;
Qun-Ji WANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Drugs, Chinese Herbal; pharmacology; Heme Oxygenase (Decyclizing); metabolism; Hypercapnia; metabolism; pathology; physiopathology; Hypertension, Pulmonary; metabolism; pathology; physiopathology; Hypoxia; metabolism; pathology; physiopathology; Male; Rats; Rats, Sprague-Dawley
- From: Chinese Journal of Applied Physiology 2002;18(1):75-79
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo study the effect of chimonin on chronic hypoxia and hypercapnic pulmonary hypertension and to explore its mechanism.
METHODSSD rats were randomly divided into normal control group (A), hypoxic hypercapnic group(B), hypoxic hypercapnia + chimonin group (C). HO-1 and HO-1 mRNA was observed in pulmonary arterioles of rats by the technique of immunohistochemistry and in situ hybridization.
RESULTS(1) mPAP was significantly higher in rats of B group than that of A and C group. Differences of mCAP were not significant in three groups. (2) Blood CO concentration was significantly higher in rats of B group than that of A group, it was significantly higher in rats of C group than that of B group. (3) Light microscopy showed that WA/TA (vessel wall area/total area), SMC (the density of medial smooth muscle cell) and PAMT (the thickness of medial smooth cell layer) were significantly higher in rats of B group than those of A and C group. (4) Electron microscopy showed proliferation of medial smooth muscle cells and collagenous fibers of pulmonary arterioles in rats of B group, and chimonin could reverse the changes mentioned above. (5) HO-1 and HO-1 mRNA in pulmonary arterioles was significantly higher in rats of B group than that of A group, they were significantly higher in rats of C group than that of B group.
CONCLUSIONChimonin can inhibit hypoxic hypercapnia pulmonary hypertension and pulmonary vessel remodeling by further increasing the expression of HO-1 mRNA.
