摘要
目的 :观察哮喘小鼠T细胞周期和bcl- 2基因表达的变化及地塞米松对它们的影响。方法 :复制小鼠过敏性哮喘动物模型 ,应用流式细胞术观察脾及肺泡灌洗液 (BALF)中T细胞数、T细胞周期和bcl- 2基因表达的变化。结果 :哮喘组脾和BALF中淋巴细胞CD3表达率显著高于对照组 ;哮喘 +地塞米松组BALF淋巴细胞中CD3表达降低 ,但脾淋巴细胞中CD3表达增高 ;哮喘组S期及G2 +M期细胞数明显多于对照组 ,同时凋亡率也高于对照组 ;哮喘 +地塞米松组S期及G2 +M期细胞数减少 ,凋亡增多 ;哮喘组T细胞bcl- 2基因表达率显著高于对照组 ,哮喘 +地塞米松对bcl- 2基因表达与哮喘组比较无明显变化。结论 :哮喘发病时 ,T细胞增多 ,脾T细胞活化增殖增加 ,凋亡增加 ,同时 ,bcl- 2基因表达率明显增加。地塞米松对哮喘的治疗作用可能并非通过抑制T细胞bcl- 2基因表达的途径。
AIM: To investigate the changes of T cell cycle, the expression of bcl-2 in allergic asthmatic mice and the effects of dexamethasone on them. METHODS: An animal model with asthma was established by means of ovalbumin sensitizing-challenging. CD3 expression in spleen and lymphocytes in bronchoalveolar lavage fluid (BALF), T cell cycle and Bcl-2 expression in spleen were detected by flow cytometry. RESULTS: In BALF lymphocytes and spleen lymphocytes, CD3 expression rate in the asthmatic group was significantly higher than that of control group. In BALF lymphocytes, CD3 expression rate in the asthma plus dexamethasone group was significantly lower than that of the asthmatic group. However, in spleen lymphocytes, CD3 expression rate in the asthma plus dexamethasone group was significantly higher than that of the asthmatic group. In spleen lymphocytes, the cell count in S phase, G 2+M phase and apoptosis rate of T cell from the asthmatic group were significantly higher than that from the control group. Cell count in S phase, G 2+M phase and apoptosis rate of T cell from the asthmaplus dexamethasone group was significantly lower than that from the asthmatic group. The Bcl-2 expression rate of T cell from the asthmatic group was significantly higher than that from the control group. CONCLUSIONS: In the allergic asthmatic mice model, T cell count, proliferation and activation of T cells, apoptosis rate of T cells in spleen lymphocytes increase, meanwhile bcl-2 expression also increases significantly. There was no significant effect of dexamethasone on the bcl-2 expression. The therapeutic effects of dexamethasone on asthma may be not due to the inhibition of the bcl-2 expression in T cells.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2004年第5期879-882,共4页
Chinese Journal of Pathophysiology
基金
广东省中医药局科研基金资助项目 (No .10 0 2 3)