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目的:观察血红素氧合酶-1(HO-1)对大鼠颈动脉球囊损伤后内膜增殖的影响。方法:健康雄性Wistar大鼠40只,随机分为4组(每组10例)。A组:正常对照组;B组:球囊损伤对照组;C组:氯血红素干预组;D组:原卟啉锌(ZnPP)干预组。A组行假手术(分离颈总动脉,但不损伤内膜),B、C、D组按文献方法制作颈动脉内膜损伤模型。B、C、D组于球囊损伤前3d至术后14d,分别给予0.9%氯化钠溶液1ml/只、氯血红素15mg/kg、ZnPP40μmol/kg隔日1次腹腔注射。球囊损伤后第14天处死大鼠,分离颈总动脉,行苏木精-伊红染色,观察颈动脉内膜增殖情况;RT-PCR及Western blotting分析颈动脉组织HO-1mRNA及蛋白质表达。结果:A组颈动脉内膜无增厚,颈动脉组织无HO-1表达;B组和D组颈动脉内膜明显增厚,D组颈动脉组织无明显HO-1表达,而B组颈动脉组织仅有少量HO-1表达;C组颈动脉内膜增厚明显减轻,HO-1表达量显著增高,与B组和D组比较差异有统计学意义(P<0.01)。结论:氯血红素显著抑制颈动脉球囊损伤后新生内膜的形成,提示HO-1在动脉损伤诱导的新生内膜形成中具有保护作用。
Objective: To observe the effect of heme oxygenase-1 (HO-1) on intima proliferation after carotid artery balloon injury in rats. Methods: Forty healthy male Wistar rats were randomly divided into 4 groups (10 in each group). Group A: normal control group; Group B: balloon injury control group; Group C: hemin intervention group; Group D: ZnPP intervention group. A group of sham operation (separation of the common carotid artery, but not damage the intima), B, C, D group according to the literature method of carotid intimal injury model. Groups B, C and D were given intraperitoneal injections of 0.9% sodium chloride solution 1 ml and hemin respectively 15 mg / kg and ZnPP 40 μmol / kg every other day for three days before balloon injury and 14 days after operation. The rats were sacrificed on the 14th day after balloon injury. The common carotid arteries were isolated and stained with hematoxylin-eosin to observe the carotid artery intima proliferation. The mRNA and protein expression of HO-1 in carotid artery were detected by RT-PCR and Western blotting. Results: There was no thickening of carotid artery in group A and no expression of HO-1 in carotid artery. In group B and D, the intima of carotid artery was significantly thicker than that of carotid artery in group A, but not in group B Arterial tissue only a small amount of HO-1 expression; C group carotid artery intimal thickening was significantly reduced, HO-1 expression was significantly increased, compared with the B group and D group was statistically significant (P <0.01). CONCLUSION: Hemin can significantly inhibit neointimal formation after carotid artery balloon injury, suggesting that HO-1 has a protective effect on neointimal formation induced by arterial injury.