摘要
目的:探讨T淋巴细胞在心肌梗死后病理性自身免疫应答中的作用。方法:将体外分离的同源大鼠脾脏树突状细胞(DC)和T淋巴细胞共培养,加入大鼠心肌肌球蛋白,使T淋巴细胞活化。将活化和未活化的T淋巴细胞分别过继转输给同源大鼠,分为转输组(接受活化T淋巴细胞)和对照组(接受未活化T淋巴细胞),观察3d、1周和4周后心肌组织病理学改变,血流动力学指标监测评价心功能状况,RT-PCR方法检测白细胞介素-1β(IL-1β)mRNA的表达。结果:转输组大鼠心肌组织有不同程度的淋巴细胞浸润,偶见心肌水肿、变性及坏死。淋巴细胞浸润以第1周最明显,呈弥漫性。对照组大鼠心肌组织未见类似病理改变。4周时转输组左心室压力最大升降率(±dp/dtmax)开始降低(P<0.05)。IL-1β mRNA表达在转输后3d开始升高,1周达到高峰,4周开始下降,且1周时心肌组织的IL-1β mRNA表达高于对照组(P<0.001)。结论:T淋巴细胞介导心肌自身免疫性炎症的发生,同时也促使心肌细胞致炎因子IL-1β的表达,共同导致急性心肌梗死后心肌细胞的损伤。
Aim : To investigate the action of T lymphocytes in the autoimmune response after acute myocardial infarction (AMI). Methods :T lymphocytes and dendritic cells were respectively purified from spleens of Lewis rats. After cocuhuring in the absence or presence of cardiac myosin (20 mg/L) , sensitized or unsensitized T lymphocytes were transferred into naive syngeneic Lewis rats by a single tail vein infusion, respectively. Recipient rats were killed at 3 day, the 1st, and 4th weekend after activated T cells transfusion to perform histopathological studies. Myocardial function was estimated by hemodynamics monitor. In addition, mRNA levels of interleukin-1β (IL-1β) in myocardial tissues were determined by RT-PCR. Results: T lymphocytes infiltration and occasional myocardium necrosis were observed in the rats after transferred activated T lymphocytes, the most markedly at the 1 st weekend and not detected in the rats of received unactivated T cells. LV pressure maximal rate of rise and fall ( ± dp/dt max) were decreased ( P 〈 0.05) at the end of the 4th weekend after received activated T lymphocytes. IL-1β were detected at 3 days, the mRNA expression were elevated significantly at 1 week and decreased at 4 weeks (P 〈 0. 001 ). Conclusion: T lymphocytes could mediate the inflammatory response and expression of IL-1β after AMI.
出处
《郑州大学学报(医学版)》
CAS
北大核心
2008年第2期245-248,共4页
Journal of Zhengzhou University(Medical Sciences)
基金
国家自然科学基金资助项目30370574