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小鼠系统性红斑狼疮样综合征的诱导及病变特征
引用本文:力弘,章蕴毅,黄晞益,孙雅楠,贾永锋,李端.小鼠系统性红斑狼疮样综合征的诱导及病变特征[J].中国新药与临床杂志,2004,23(8):480-484.
作者姓名:力弘  章蕴毅  黄晞益  孙雅楠  贾永锋  李端
作者单位:复旦大学药学院,药理教研室,上海,200032
摘    要:目的 :用ConA活化淋巴细胞的染色质免疫小鼠 ,建立稳定的系统性红斑狼疮 (SLE)样自身免疫反应亢进小鼠模型 ,并进一步观察模型的各项改变。方法 :ConA活化的BALB/c小鼠脾细胞中提取活性染色质。每只以染色质 10 0 μg在d 0 ,14 ,2 8背部皮内注射免疫小鼠 3次 ,建立SLE样自身免疫反应亢进小鼠模型。用ELISA方法测定免疫后血清中抗自身抗体、总IgG的动态生成情况 ;用Hep 2细胞作抗核抗体核型检测。用考马斯亮蓝法测定小鼠尿蛋白含量 ;对小鼠肾脏做病理检查。用硝酸还原酶比色法测定血清一氧化氮 (NO)含量 ,用ELISA方法测定LPS诱导腹腔巨噬细胞产生肿瘤坏死因子 (TNF α)的水平。用 5 0 %溶血试验法测定血清中总补体含量。进行了红细胞、白细胞、血小板计数。结果 :模型小鼠血清抗核抗体 ,总IgG ,NO水平均升高 ,补体下降 ,血象中血小板减少 ,抗核抗体核型为均质型和胞浆型。小鼠有狼疮样肾炎 ,尿蛋白 ,腹腔巨噬细胞TNF α产生减少。结论 :自身活化染色质诱导的SLE样综合征小鼠模型具有与SLE类似病变。

关 键 词:自身免疫疾病  红斑狼疮  系统性  染色质  抗体  抗核  肿瘤坏死因子  一氧化氮  补体  动物  实验
文章编号:1007-7669(2004)08-0480-05

Induction and characteristics of systemic lupus erythematous syndrome in mice
LI Hong,ZHANG Yun-yi,HUANG Xi-yi,SUN Ya-nan,JIA Yong-feng,LI Duan.Induction and characteristics of systemic lupus erythematous syndrome in mice[J].Chinese Journal of New Drugs and Clinical Remedies,2004,23(8):480-484.
Authors:LI Hong  ZHANG Yun-yi  HUANG Xi-yi  SUN Ya-nan  JIA Yong-feng  LI Duan
Abstract:AIM: To establish the stable lupus-like syndrome(SLE) model in the BALB/c mice and observe the changes of the model. METHODS: BALB/c mice were immunized with syngenetic active chromatin 100 μg per mice on d 0,d 14 and d 28 to establish SLE-like model. The presence of anti-nuclear antibodies and total IgG were measured in enzyme-linked immunosorbent assays (ELISA). Hep-2 cells were used to detect the patterns of antinuclear antibodies. Nitric oxide (NO) and complement level in serum was measured. Peritoneal cells were cultured and tumor necrosis factor-α (TNF-α) in supernatants was detected in ELISA. Proteinuria was measured and kidneys were examined by light microscopy. Red cells,white cells,platelets were counted. RESULTS: The active chromatin immunized mice demonstrated that levels of autoantibodies,total IgG and NO increased. Thrombocytopenia appeared and complement level reduced,the pattern of antinuclear antibodies was homogeneous and cytoplasmic. Kidney was evaluated histologically. TNF-α production was lower and proteinuria was higher in active chromatin treated mice. CONCLUSION: Experimental SLE in mice can be induced by active chromatin immunization.
Keywords:autoimmune diseases  lupus erythematosus  systemic  chromatin  antibodies  antinuclear  tumor necrosis factor  nitric oxide  complement  animals  laboratory
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