胶原诱导性关节炎小鼠存在血管内皮功能失调——类风湿关节炎加速动脉粥样硬化的新证据

Collagen-induced Arthritis Mice Existed Endothelial Dysfunction ---- The New Evidence of Rheumatoid Arthritis Accelerated Atherosclerosis

目的类风湿关节炎(RA)患者易患动脉粥样硬化(AS),而RA是否会造成内皮功能障碍,并通过该途径触发或者加速AS是我们的研究重点。方法观察胶原诱导性关节炎(CIA)小鼠及同期对照小鼠的主动脉对于乙酰胆碱及硝普纳诱导的血管舒张率并进行对比,及CIA与对照小鼠血管组织iNOS及eNOS表达水平的检测。结果对照小鼠的主动脉组织中,对于乙酰胆碱的诱导,血管舒张率为88.70±22.90%,CIA显著下降为53.90±18.40%(p<0.01)。对于硝普纳的诱导则未见差异。CIA小鼠血管组织中eNOS表达下调,iNOS表达升高。结论 CIA小鼠存在内皮细胞功能障碍且与关节炎严重程度呈正相关。

Object ive To detect ive whether rheumatoid arthrit is(RA)cou ld cause dys function of end othelium and accelerate pro gress of atherosclerosis(AS)through dysfunct ion as pat ients of RA patients are liable to AS.Meth ods Detect ion and comparison of vasodilatat ion rate of aorta to acety lchol ine and sodium nitroprusside and expression level of iNOS and eNOS in vess el of collagen-induced arthrit is(CIA)mice and the same age control mice.Results Vasodilatation rate of aorta to acetylchol ine was 88.70±22.90% in control mice whi le that in CIA mice decreased to 53.90±18.40%(p<0.01)No signi��cant differences between two groups to sodium nitroprus side. Expression level of eNOS decreas ed whi le iNOS increased in ves sel in CIAmice.Con clusion Endothel ium dysfunct ion existed in CIAmice and posi tive correlation with s everi ty of RA.