| ObjectiveAbdominal aortic aneurysm ( AAA) is a common disease in vascular surgery and is characterized by localized structural deterioration of aortic wall, leading to progressive aortic dilation and eventual rupture. The mobidity of AAA is increasing with aging. Multiple reasons are responsible for the formation and development of aneurysmal degenerative disease, including the degradation of elas-tin and collagen; increased level of matrix metalloproteinase (MMP) ; inflammatory infiltration; apoptosis of smooth muscle cell (SMC). Genetic factor, im-muno - factor, chemical factor and hemodynamic factor are all play important roles in the formation of aneurysms. At present, the pathogenesis of AAA isn't fully clear. So further research into the mechanism of AAA appears profound importance.Heme oxygenase ( HO) catalyzes the initial and rate - limiting step in heme metabolism. It oxidatively degrades heme into equimolar amounts of carbon monoxide (CO) , free iron and biliverdin. Biliverdin is subsequently metabolized to the potent antioxidant bilirubin by biliverdin reductase.In this paper, we will establish experimental abdominal aortic aneurysm model in rats, observing the dynamic expression of HO-1. Furthermore, explore the role of HO-1 in the formation of AAA by treatment with HO-1 inducer, he-min.Method68 Wistar rats were divided into 4 groups randomly; surgery group (S group) , normal control group, hemin treatment group ( H group) and saline treatment group ( N group) , and experimental AAA model was made by elastaseperfusion. In S group, the specimens were harvested at postoperative day 3,7, 14, 28. HE staining and Verhoeff-van Gieson staining were used to observe the elastic fiber disruption and inflammatory cell infiltration, and in tisu hybridization was applied to detect the expression of HO-1 in aortic wall. In H and N group, the specimen was obtained at postoperative day 7, 14, and the dilatation rate was calculated. The expression of ICAM-1 and HO-1 were detected by im-munohistochemical staining.ResultsAbnominal aorta dilated slightly after PPE perfusion in all group, which didn' t show signifant difference ( P > 0. 05 ). After perfusion, the dilation increased and formed experimental AAA model at POD 7. But in hemin pretreat-ment group ( H group) , the aorta dilation was inhibitated obviously and it did * t form AAA model, which showed signifant difference compared with N group (P <0.01).In situ hybridization staining of HO-1mRNA; the expression was negative in normal aorta; In S group, positive expression was seen at POD 3, and it reached the peak at POD 14, which showed significant difference compared with other time phase( P <0. 01).Immunohistochemical staining of ICAM-1 and HO-1: In N group, ICAM-1 protein strongly expressed at POD 7, and the percentage of positive area was 10.4% , locating in tunica media and proliferated intima. At POD 14, the expression of ICAM-1 weakened, locating in the adventitia. In H group, the expression of ICAM-1 was inhibitated (P <0. 01, H group vs N group). The expression of HO-1 was seen in both N and H group, but the percentage of positive area in H group was higher than that in N group (P <0.05).ConclusionThe expression of HO-1 was increased in experimental abdominal aortic an-eurismal tissue and was associated with elastin disruption and inflammatory infil-tration in aortic wall, suggesting that HO-1 may exert protective anti - inflammatory effects to the formation and development of AAA. The dilation of AAA was inhibitated by HO-1 inducer, hemin. One of the protective anti - inflammatory mechanisms was practiced by the inhibition of ICAM-1 expression.
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