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为探讨细胞凋亡机制在乙酰胆碱受体抗体(AchRab)脑室内注射致重症肌无力(MG)中枢神经系统(CNS)受损的可能机制,将MG患者血中提取的AchRab经侧脑室注射到大鼠脑室系统,建立CNS受损的MG大鼠模型。用免疫细胞化学法观察CNS中Fas/FasL、Bcl-2、Bag-1的表达,用原位末端标记(TUNEL)的方法观察脑细胞凋亡情况及不同病程变化,并与用健康人血清提取的lgG注入大鼠侧脑室建立的对照组进行比较;另一组不予任何处理怍为空白对照。结果表明,MG模型大鼠表现出类似实验性自身免疫性重症肌无力(EAMG)动物模型样症状;MG组Fas/FasL抗原主要表达于大脑皮质和海马神经元薄膜和突起,而对照组抗原的表达则阴性,两组Bcl-2和Bag-1表达差异无显著意义;TUNEL结果示实验组大鼠脑组织切片阳性细胞于注射后第2周出现,且随时间推移逐渐增多,至第3周后数目最多。脑内多部位都有凋亡细胞出现,以皮质和海马区较明显,与对照组比较,差别明显。结论:Fas/Fasl,参与AchRab引起大鼠CNS功能障碍过程,细胞凋亡在此损害中可能起重要作用。
AchRab extracted from the blood of MG patients was injected into the lateral ventricle to induce apoptosis of the central nervous system (CNS) induced by intracerebroventricular injection of acetylcholine receptor antibody (AchRab) in order to explore the mechanism of apoptosis. Rat ventricular system, establish CNS damaged MG rat model. The expressions of Fas / FasL, Bcl-2 and Bag-1 in CNS were observed by immunocytochemical method. The apoptotic cells and different course of apoptosis were observed by TUNEL method. Of lgG injection into the rat lateral ventricle to establish the control group were compared; the other group without any treatment 怍 as a blank control. The results showed that MG model rats showed similar experimental animal model-like symptoms of autoimmune myasthenia gravis (EAMG). The Fas / FasL antigens of MG group were mainly expressed in the membrane and protrusions of neurons in the cerebral cortex and hippocampus, The expression of Bcl-2 and Bag-1 in the two groups had no significant difference. The results of TUNEL showed that in the experimental group, positive cells of brain tissue section appeared in the second week after injection, and gradually increased with the passage of time. By the third week After the largest number. Apoptotic cells appeared in many parts of the brain, with cortical and hippocampal areas more obvious, compared with the control group, the difference was significant. Conclusion: Fas / Fasl participates in the process of CNS dysfunction induced by AchRab, and apoptosis may play an important role in this damage.