血管外膜介导的炎症反应对血管平滑肌细胞增殖的影响  

Effects of inflammatory reaction mediated by adventitia on the proliferation of vascular smooth muscle

作　　者：牟华明[1] 王利娟[1] 闫振成[1] 曹廷兵[1] 祝善俊[1] 祝之明[1] 

机构地区：[1]第三军医大学全军高血压代谢病中心重庆市高血压研究所第三军医大学大坪医院高血压内分泌科,重庆400042

出　　处：《解放军医学杂志》2007年第7期734-737,共4页Medical Journal of Chinese People's Liberation Army

摘　　要：目的观察血管外膜介导的炎症反应对血管平滑肌细胞(VSMC)增殖的影响,并探讨其机制。方法采用兔颈动脉外膜组织与平滑肌细胞共培养方法,分以下6组,①单独培养组:培养的VSMC中不加外膜组织及药物;②单独培养+脂多糖(LPS,1μg/ml)组;③单独培养+LPS+N-硝基-L-精氨酸甲酯(L-NAME,100mmol/L)组;④复合培养组:培养的VSMC中加入外膜组织块;⑤复合培养+LPS组;⑥复合培养+LPS+L-NAME组。用氚-胸腺嘧啶(3H-TdR)检测各组VSMC增殖状态,试剂盒测定培养液中抗超氧阴离子自由基及亚硝酸盐(NO2-)含量,蛋白免疫印迹法检测血红素加氧酶-1(HO-1)蛋白表达。结果与单独培养组比较,LPS刺激前,复合培养组VSMC3H-TdR掺入率、NO2-含量无明显差异,抗超氧阴离子活力单位增高(P<0·05),HO-1蛋白表达显著增加(P<0·01);LPS刺激后,复合培养+LPS组VSMC3H-TdR掺入率显著降低(P<0·01),抗超氧阴离子活力单位显著增高(P<0·01),NO2-含量增高(P<0·05),HO-1蛋白表达显著增加(P<0·01);复合培养+LPS+L-NAME组VSMC3H-TdR掺入率、NO2-含量、HO-1蛋白表达无明显差异,抗超氧阴离子活力单位显著增高(P<0·01)。结论血管外膜可通过一氧化氮(NO)及HO-1等途径抑制LPS刺激所致的VSMC增殖。Objective To observe the effects of inflammatory reaction mediated by adventitia on the proliferation of vascular smooth muscle cells （VSMC） and to elucidate the relevant mechanisms. Methods Six groups of rat carotid artery adventitia and VSMC were cocultured and incubated for 24 hours： Group 1, VSMC alone, no adventitia and pharmaceuticals were added; Group 2, VSMC incubated with 1μg/ml lipopolysaccharide （LPS）; Group 3, VSMC incubated with 1μg/ml LPS and 100mmol/L L-NAME; Group 4, co-culture of adventitia and VSMC; Group 5, co-culture of VSMC and adventitia with addition of 1μg/ml LPS; and Group 6, co-culture of VSMC and adventitia with addition of 1μg/ml LPS and 100mmol/L L-NAME. The proliferation of VSMC in each group was measured by 3^HTdR incorporation; the contents of anti-superoxide anion radical and nitric oxide （NO） production （NO2^- ） were determined by use of specific reagents; and the level of heine oxygenase-1 （HO-1） was determined by Western blot. Results No difference in 3^H-TdR incorporation of VSMC and NO2^- was found in co-culture groups compared with that in VSMC alone group. The anti superoxide anion radical and HO1 expression in co-cultured group were significantly increased compared with that in VSMC group （ P〈0.05 or P〈0. 01）. When stimulated by LPS, the 3^H-TdR incorporation of VSMC in co-cultured group was significantly decreased （ P〈0. 01）, while the anti-superoxide anion radical and NO2^- were increased sharply with the up-regulation of HO1 expression compared with that in VSMC group （P〈0.05 or P〈 0. 01）. After incubated with L-NAME and LPS, only the anti-superoxide anion radical in co-cultured group increased compared with that in VSMC group. Conclusion Mediated by NO and HO-1, the vascular adventitia may inhibit the proliferation of VSMC induced by LPS.

关 键 词：血管外膜 肌 平滑 血管 一氧化氮 血红素氧化酶-1 

分 类 号：R543[医药卫生—心血管疾病]