血管紧张素Ⅱ1型受体自身抗体对VCAM-1的表达影响

Impact on the Expression of VCAM-1 Autoantibody against Angiotensin Ⅱ Type 1 Receptor(AT1-AA)

目的:观察血管紧张素Ⅱ1型受体自身抗体(AT1-AA)长期作用下,大鼠血管内皮细胞血管细胞黏附分子-1(VCAM-1)的表达影响。方法:以合成的人AT1R的细胞外第二环功能肽段为抗原,主动免疫Wistar雌性大鼠9个月,建立AT1-AA高滴度的大鼠模型,以免疫组织化学染色法检测血管内皮细胞血管细胞黏附分子-1的表达。结果:主动免疫的Wistar雌性大鼠,从免疫2个月开始直到免疫结束,血清中产生了高滴度并维持恒定的AT1-AA(免疫9个月时光密度值vs.同期对照组为1.79±0.26vs.0.43±0.15,P<0.05,)。在免疫结束时,大鼠胸主动脉内皮细胞血管细胞黏附分子-1(免疫组平均光密度值vs.同期对照组为0.27±0.04 vs.0.17±0.04,P<0.05)表达显著上调。结论:在AT1-AA的长期刺激下引起大鼠血管内皮细胞VCAM-1升高,从而引起血管内皮炎性反应,这对AT1-AA在先兆子痫发病机制中的研究中具有重要意义。

Objective：To investigate whether autoantibody against angiotensin Ⅱ type 1 receptor（AT1-AA） can impact the expression of VCAM-1.Methods：To establish AT1-AA-positive rat models,health adult female Wistar rats were actively immunized with the synthetic peptide corresponding to AT1R-ECⅡ for nine months.Immunohistochemical method was used to determine the level of vascular cellular adhesion molecule-1（VCAM-1） in vascular endothelial cells.Results：From the second month after the primary immune to the end of the experiment,the titer of AT1-AA maintained at a constant high level（optical density value at 9 month was 1.79 ± 0.26 vs 0.43 ± 0.15,P〈0.05,vs vehicle group）.At 9 month,VCAM-1（mean optical density,0.27 ± 0.04 vs.0.17 ± 0.04,P〈0.05） were markedly increased in vascular endothelium.Conclusion：The long-term stimulation with AT1-AA can induce the VCAM-1 rise,causing the endothelial inflammatory reaction,which is of great significance in the pathogenesis of preeclampsia in the AT1-AA study.