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探讨球囊损伤后血管重塑中血红素氧合酶-1(HO-1)/一氧化碳(CO)系统与一氧化氮合酶(NOS)/一氧化氮(NO)系统的作用及相互关系。家兔随机分为对照组、假手术组、胆固醇组、精氨酸组、亚硝基组、血红素组和卟啉锌组。对照组喂普通饲料,其余六组喂含1.5%胆固醇饲料,精氨酸组和亚硝基组饮水同时予L-精氨酸或亚硝基-L-精氨酸甲酯,血红素组和卟啉锌组同时分别予氯化血红素或锌原卟啉-9腹腔内注射。2周后实验组行一侧颈总动脉球囊损伤,术后续原喂养给药8周。结果显示:与胆固醇组比较,血红素组HO活性、CO生成量显著增加,核因子κB活性显著降低,内膜面积显著减小(均P<0.01);卟啉锌组呈现相反的结果;精氨酸组cNOS活性、NO生成量显著增加,核因子κB活性显著降低,内膜面积显著减小(均P<0.01);亚硝基组cNOS活性、NO生成量显著降低,核因子κB活性显著升高(均P<0.01),内膜面积变化无显著性。本研究表明,再狭窄形成中HO-1/CO与NOS/NO两系统显示互补及代偿作用,HO-1/CO系统可能通过对NOS/NO系统的代偿和调节并抑制核因子κB活性,从而抑制血管损伤后内膜增殖及负性重塑。
To investigate the role and relationship of HO-1 / CO and NOS / NO in vascular remodeling after balloon injury. Rabbits were randomly divided into control group, sham operation group, cholesterol group, arginine group, nitroso group, heme group and porphyrin zinc group. Control group fed normal feed, the other six groups fed with 1.5% cholesterol feed, arginine group and nitroso group drinking water to L-arginine or nitroso-L-arginine methyl ester, heme group and Porphyrin zinc group were simultaneously hemin or zinc protoporphyrin-9 intraperitoneal injection. Two weeks later, the common carotid arteries in one side of the experimental group were inflicted with balloon injury. The results showed that compared with the cholesterol group, the HO activity and the CO production were significantly increased, the activity of nuclear factor κB was significantly decreased and the intimal area was significantly decreased (all P <0.01) The activity of cNOS, the production of NO and the activity of nuclear factor kappa B were significantly decreased (P <0.01). The activity of cNOS and the production of nitric oxide were significantly decreased and the activity of nuclear factor κB was significantly increased (All P <0.01), no significant change of intima area. The present study shows that HO-1 / CO and NOS / NO show complementary and compensatory roles in restenosis formation. HO-1 / CO system may compensate and regulate NOS / NO system and inhibit nuclear factor κB activity , Thereby inhibiting intimal proliferation and negative remodeling after vascular injury.