摘要
目的探讨重症肌无力(myastheniagravis,MG)的发病机制,为临床治疗提供一定的实验理论依据。方法用机械分离法、淋巴细胞分离液获取19例MG患者和11例正常对照组胸腺细胞悬液,接种于培养板中,分别加入雌、孕激素作为特异性刺激组,未加内分泌激素作为空白对照组,培养72h后收获细胞。采用流式细胞术分别检测MG患者和正常对照组胸腺细胞及雌、孕激素培养前后胸腺细胞的Bcl-2表达。结果MG患者胸腺细胞Bcl-2表达率比正常对照组显著增高,2者相比有统计学意义(P<0.01);雌、孕激素培养组MG患者胸腺细胞Bcl-2的表达率比空白对照组显著降低,分别比较差异有统计学意义(P<0.05),雌激素培养组与孕激素培养组比较差异无统计学意义(P>0.05)。结论MG患者胸腺细胞Bcl-2表达升高,可能参与调控胸腺细胞凋亡,其表达异常可能是MG发病的一个重要因素;雌、孕激素抑制MG患者胸腺细胞Bcl-2的表达,提示体内雌激素、孕激素水平变化与MG患者病情变化有一定联系。
Objective To explore the pathogenesis of myasthenia gravis (MG) and provide some theorical basis to therapy. Methods Thymocytes were obtained from the thymus in 19 patients with MG and 11 normal controls. The cell suspension was subcultured in the culture template. Estrogen, progesterone were separately added as experimental groups, nothing was added as blank control. Thymocytes were harvested after 72 hours. The expression of Bcl-2 in pro-cultured and post-cultured thymocytes and the rates of thymoeyte apoptosis after culture in the presence of each hormone were detected by flow eytometry (FCM). Results Bcl-2 protein expressed in thymocytes was significantly higher in MG patients than in normal controls(P〈0.01); The positive rates of Bcl- 2 protein expression in thymocytes of MG patients were significantly higher in groups of estrogen, progesterone culture than in normal controls(P〈0. 05). However, there was no significant difference under cultures in the presence of estrogen or progesterone culture(P〉0. 05). Conclusion The expression of Bcl-2 in the thymocyte in patients with MG is upregulated, which probably participates in controlling the thymocyte apoptosis. This may be one of important factors in the pathogenesis of MG; Estrogen and progesterone inhibit the expression of Bel-2 in the thymocytes in patients with MG; There is probably a relation between the change of the level of Estrogen and progesterone and the different disease conditions in patients with MG.
出处
《中国实用神经疾病杂志》
2007年第1期23-25,共3页
Chinese Journal of Practical Nervous Diseases
基金
国家自然科学基金资助项目30570625
河南省杰出青年科学基金0212000100