Document Detail


Effect of the haeme oxygenase-1/endogenous carbon monoxide system on atherosclerotic plaque formation in rabbits.
MedLine Citation:
PMID:  20972512     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: To investigate the effect of the haeme oxygenase-1/carbon monoxide (HO-1/CO) system on atherosclerotic plaque formation and its possible mechanism.
METHODS: For 12 weeks, rabbits were given a 1.5% cholesterol diet (Ch group, n = 8) or a 1.5% cholesterol diet plus an HO-1 inducer, haemin (Hm group, n = 8), or an HO-1 inhibitor, zinc protoporphyrin IX (Znpp-IX, Zn group, n = 8) by intraperitoneal injection.
RESULTS: Compared with the normal control group (C group, n = 8), serum levels of lipids and oxidised low-density lipoproteins (ox-LDL) increased significantly in all experimental groups (p < 0.01). However, no significant differences were observed among the three experimental groups (p > 0.01). Compared with the control group, aortic nitric oxide (NO) production and nitric oxide synthase (cNOS) activity decreased markedly, whereas carbon monoxide (CO) production and HO-1 activity increased markedly in the Ch group (p < 0.01). This was associated with an increase in the area of aortic plaque of 54.00 ± 4.16%. Compared with the Ch group, CO production and HO-1 activity increased markedly, while aortic HO activity and CO production decreased significantly in the Hm group. The area of aortic plaque was significantly reduced in the Hm group (17.88 ± 3.01%), whereas the area of aortic plaque was significantly increased in the Zn group (61.13 ± 3.50%). Compared with the Ch group, aortic endothlin-1 expression in the Hm group reduced significantly, while in the Zn group it was significantly higher than in the Ch group (p < 0.01).
CONCLUSION: The HO-1/CO system plays an inhibitory role in atherosclerotic plaque formation. This role was not mediated by regulating serum lipids and ox-LDL, but was related to the reciprocal relationship between the HO-1/CO and NOS/NO systems in atherosclerosis and the down-regulated expression of endothlin-1 (ET-1), which inhibits the proliferation of vascular smooth muscle cells.
Authors:
Da-Nan Liu; Ying Fang; Li-Rong Wu; Xing-De Liu; Ping Li; Zuo-Yun He
Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Cardiovascular journal of Africa     Volume:  21     ISSN:  1995-1892     ISO Abbreviation:  Cardiovasc J Afr     Publication Date:    2010 Sep-Oct
Date Detail:
Created Date:  2010-10-25     Completed Date:  2011-01-04     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101313864     Medline TA:  Cardiovasc J Afr     Country:  South Africa    
Other Details:
Languages:  eng     Pagination:  257-62     Citation Subset:  IM    
Affiliation:
Department of Cardiology, Guiyang Medical College, Guiyang, China. yi_yi0809@126.com
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MeSH Terms
Descriptor/Qualifier:
Animals
Aorta / cytology,  pathology
Carbon Monoxide / physiology*
Cell Proliferation
Down-Regulation / physiology
Endothelin-1 / metabolism
Heme Oxygenase-1 / antagonists & inhibitors,  metabolism,  physiology*
Immunohistochemistry
Muscle, Smooth, Vascular / metabolism
Nitric Oxide Synthase / metabolism
Plaque, Atherosclerotic / pathology,  physiopathology*
Protoporphyrins / pharmacology
Rabbits
Chemical
Reg. No./Substance:
0/Endothelin-1; 0/Protoporphyrins; 15442-64-5/zinc protoporphyrin; 630-08-0/Carbon Monoxide; EC 1.14.13.39/Nitric Oxide Synthase; EC 1.14.99.3/Heme Oxygenase-1

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