摘要
目的:研究中药狼疮方对狼疮样BXSB小鼠免疫系统和淋巴细胞亚群的影响,探讨狼疮方治疗SLE的免疫学机制。方法:采用BXSB小鼠模型,随机分为3组:狼疮方治疗组(每天0.5mL狼疮方药液灌胃)、强的松治疗组(每天prednisone0.173mg/20gBW溶于0.5mL生理盐水灌胃),未治疗组(每天0.5mL生理盐水灌胃),每组6只,疗程10周。另设与BXSB小鼠同基因的正常C57BL/6小鼠6只为正常对照组。分别采集上述各组小鼠外周血和脾组织进行检测。结果:(1)未治疗组BXSB小鼠血清IgG和抗ds-DNA抗体水平及脾组织CD3、CD4、CD8、CD19、CD23阳性细胞百分比都显著高于正常对照组、狼疮方治疗组、强的松治疗组(P<0.05或P<0.01)。(2)经狼疮方或强的松治疗后,BXSB小鼠血清IgG、抗ds-DNA抗体水平及脾组织CD4、CD8、CD19、CD23阳性细胞百分比显著低于未治疗组(与未治疗组相比,P<0.05或P<0.01),且接近正常水平(与正常对照组比较,P>0.05)。结论:狼疮样BXSB小鼠T、B细胞免疫功能上调。中药狼疮方可抑制狼疮样小鼠T、B淋巴细胞活化,减轻其高丙种球蛋白血症,减少体内自身抗体产生。
AIM: To investigate the effects of lupus recipe on immune system and lymphocyte subsets proliferation in splenic cells in BXSB mice. METHODS: Eighteen male BXSB mice model was used in the experiment. The model mice were divided into three groups: un-treated model group, lupus recipe (LR) treated group, and prednisone treated group. All model mice were killed in 10 weeks. The control group consisted of 6 syngeneic normal C57BL/6 male mice. The levels of total IgG and anti - dsDNA antibody in serum were detected by ELISA. The percentages of lymphocyte subsets ( CD3^+ , CD4^+ , CD8^+ T lymphocytes and CD19^+ , CD23^+ B lymphecytes) were detected by using flow cytometry analysis. RESULTS: (1) The serum levels of total IgG and anti - dsDNA antibody in un- treated model group were higher than that in other groups. There was no differences among LR treated group, prednisone treated group and control group. (2) The percentages of CD3^+ , CD4^+ , CD8^+ T lymphocytes and CD19^+ , Cd23^+ B lymphocytes in model group were obviously higher than that in normal control. (3) Compared to un- treated model group, the percentages of CD4^+ , CD8^+ T lymphecytes and CD19^+ , CD23^+ B lymphecytes in LR or prednisone treated group were significantly reduced, which closely reached the levels in normal group. CONCLUSIONS: The immune functions of T and B lymphocytes in BXSB mice are up - regulated. LR inhibits the activation of T and B lymphocytes, reduces the serum levels of IgG and auto- antibody production.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2006年第3期551-554,共4页
Chinese Journal of Pathophysiology
基金
中山医科大学211工程重点科研基金资助项目(No.98151)