| Effect of the haeme oxygenase-1/endogenous carbon monoxide system on atherosclerotic plaque formation in rabbits. | |
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MedLine Citation:
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PMID: 20972512 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Da-Nan Liu; Ying Fang; Li-Rong Wu; Xing-De Liu; Ping Li; Zuo-Yun He |
Publication Detail:
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Type: In Vitro; Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Cardiovascular journal of Africa Volume: 21 ISSN: 1995-1892 ISO Abbreviation: Cardiovasc J Afr Publication Date: 2010 Sep-Oct |
Date Detail:
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Created Date: 2010-10-25 Completed Date: 2011-01-04 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101313864 Medline TA: Cardiovasc J Afr Country: South Africa |
Other Details:
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Languages: eng Pagination: 257-62 Citation Subset: IM |
Affiliation:
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Department of Cardiology, Guiyang Medical College, Guiyang, China. yi_yi0809@126.com |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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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:
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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 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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