CAJ | 학술논문

目的探讨T淋巴细胞及其亚群在腹主动脉瘤发病中的作用.方法 50只Wistar大鼠随机分成A、B、C、D、E5组,每组10只,A组为正常对照组,B、C、D、E组分别为术后3、7、14、28 d组,运用猪胰弹力酶灌注法建立腹主动脉瘤模型.免疫组化方法检测上述各组大鼠腹主动脉局部T、B淋巴细胞及巨噬细胞的表达水平,流式细胞术检测各组大鼠外周血中CD4+ CD28-T淋巴细胞亚群的分布变化.结果大鼠腹主动脉局部T、B淋巴细胞及巨噬细胞表达的变化:术后7dT细胞显著升高(40±15,P＜0.05),B细胞及巨噬细胞有升高,但差异无统计学意义(P＞0.05)；术后14 d,3种细胞表达升高最为显著(P＜0.05)；术后28 d,3种细胞的表达较术后14 d明显下降.术后各组大鼠外周血CD4+、CD28-T细胞均有升高(P＜0.05),以术后7d比例最高(8.1％±2.1％,P＜0.05).结论 T淋巴细胞是腹主动脉瘤形成过程中最重要的炎症细胞之一,T淋巴细胞的浸润及其亚群分布变化所致的免疫及炎症反应在腹主动脉瘤形成早期可能起着重要的触发及调节作用.
목적 탐토T림파세포급기아군재복주동맥류발병중적작용.방법 50지Wistar대서수궤분성A、B、C、D、E5조,매조10지,A조위정상대조조,B、C、D、E조분별위술후3、7、14、28 d조,운용저이탄력매관주법건립복주동맥류모형.면역조화방법검측상술각조대서복주동맥국부T、B림파세포급거서세포적표체수평,류식세포술검측각조대서외주혈중CD4+ CD28-T림파세포아군적분포변화.결과 대서복주동맥국부T、B림파세포급거서세포표체적변화:술후7dT세포현저승고(40±15,P＜0.05),B세포급거서세포유승고,단차이무통계학의의(P＞0.05)；술후14 d,3충세포표체승고최위현저(P＜0.05)；술후28 d,3충세포적표체교술후14 d명현하강.술후각조대서외주혈CD4+、CD28-T세포균유승고(P＜0.05),이술후7d비례최고(8.1％±2.1％,P＜0.05).결론 T림파세포시복주동맥류형성과정중최중요적염증세포지일,T림파세포적침윤급기아군분포변화소치적면역급염증반응재복주동맥류형성조기가능기착중요적촉발급조절작용.
Objective To evaluate T cell and CD4+ CD28-T in the development and progression of abdominal aortic aneurysms (AAAs).Methods Fifty Wistar rats were randomly divided into 5 groups (n =10 each).An AAA animal model is established by enhancing perfusing elastase to the infrarenal abdominal aorta of the rats.The levels of T cell,B cell and macrophage cell of abdominal aorta of the rats on days 3,7,14 and 28,were detected by enzyme linked immunosorbent assay(ELISA).CD4+ CD28-T cell of the peripheral blood were measured by flow cytometry.Result There was significant T-lymphocyte infiltration both in middle and outer membrane of the artery of the rats on day 7 after surgery.T-lymphocyte,B-lymphocyte and macrophage cell infiltration were on the peak in middle and outer membrane of the artery on day 14 after surgery.The ratio of CD4+ CD28-T cell in rat peripheral blood reached peak on day 7(P ＜0.05).Conclusions T cell and CD4+ CD28-T cell expression increased in peripheral blood and abdominal aorta in AAA rat model,suggesting a potential role of T cell and CD4+ CD28-T cells in the pathogenesis of AAAs,especially during the early development of AAAs.