Protective effect of heme oxygenase-1-endogenous carbon monoxide system on restenosis after balloon injured rabbit carotid artery / 中华老年医学杂志
Chinese Journal of Geriatrics
; (12): 232-236, 2011.
Article
em Zh
| WPRIM
| ID: wpr-413894
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WPRO
ABSTRACT
Objective To investigate the protective effect of heme oxygenase-1 (HO-1)/carbon monoxide (CO) system on restenosis after balloon angioplasty and relative mechanism. Methods Fifty rabbits were randomly divided into 5 groups. Control group received normal chow (Control group), the other rabbits received 1.5% cholesterol diet (Chol group and SH group) or 1.5%cholesterol diet plus hemin (Hem group) or zinc protoporphyrin Ⅸ (Znpp group) for 10 weeks. At the third week of experiment, the three experimental groups underwent balloon injury at one side common carotid artery. Results Compared with control group, arterial nitric oxide production and nitricoxide synthase activity were significantly decreased, while HO-1 expression and CO production were significantly increased (all P<0. 01 ) in Chol group. The intima thickness and ratio of intima/media (I/M) were lower in Hem group than in Chol group [(281.47± 21.10) μm vs. (442.17 ±59.14) μm, 2.49 ± 0. 17 vs. 3.99 ± 0. 52, respectively]. While arterial HO-1 expression and CO production were increased markedly, endothelin-1 expression was distinctly reduced in Hem group group than in Chol group. Compared with Chol group, arterial HO-1 expression and CO production were decreased obviously, while endothelin-1 expression and intima thickness and ratio of intima/media [(698.71±58. 37) μm, 6.17±0. 52]were significantly increased in Znpp group (all P<0. 01).Conclusions The HO-1/CO system plays a protective role on improving endothelium function and restraining neointimal proliferation by compensating and regulating nitricoxide synthase/nitric oxide system and lowering endothelin -1 expression so as to inhibit restenosis after balloon injury.
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Base de dados:
WPRIM
Idioma:
Zh
Revista:
Chinese Journal of Geriatrics
Ano de publicação:
2011
Tipo de documento:
Article