论文部分内容阅读
为观察重症肌无力中胸腺细胞凋亡的变化 ,制备了实验性自身免疫性重症肌无力 (EAMG )模型 ,采用切口及末端标记 (TUNEL )的方法观察了病程的不同阶段中胸腺细胞的凋亡情况。结果表明 ,EAMG的胸腺出现了细胞凋亡指数的减少 ,在免疫后第 4周 ,细胞凋亡指数减少最明显 (P <0 0 1)。进一步观察 ,可见实验鼠从第 4周开始 ,EAMG胸腺中Bcl 2的表达增加 ,而且细胞凋亡指数的减少与Bcl 2表达分数的增加呈明显的负相关。由此可见Bcl 2表达的增加 ,可导致EAMG胸腺中激活免疫细胞的正常凋亡过程抑制 ,可能是MG自身免疫发病机制之一。
To observe the changes of thymocyte apoptosis in myasthenia gravis, an experimental autoimmune myasthenia gravis (EAMG) model was prepared. The apoptosis of thymus cells in different stages of the course of the disease was observed by means of incision and terminal labeling (TUNEL) Happening. The results showed that there was a decrease of apoptotic index in the thymus of EAMG. The apoptosis index decreased most significantly in the 4th week after immunization (P <0.01). Further observation showed that from the 4th week onwards, the expression of Bcl 2 in EAMG thymus increased, and the decrease of apoptosis index was negatively correlated with the increase of Bcl 2 expression score. Thus, the increase of Bcl-2 expression can lead to the inhibition of the normal apoptosis process of activated immune cells in the thymus of EAMG, which may be one of the pathogenesis of MG autoimmunity.