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作 者:许倬[1] 韩星海[1] 管剑龙[1] 闾坚强[1] 蔡青[1] 田野苹[2] 施冶青[1]
机构地区:[1]第二军医大学长海医院风湿免疫科,上海200433 [2]基础医学部免疫学教研室
出 处:《第二军医大学学报》2003年第7期791-794,共4页Academic Journal of Second Military Medical University
摘 要:目的 :研究 α黑素细胞刺激素 (α- melanocyte- stim ulating horm one,α- MSH)对大鼠胶原性关节炎 (collagen- inducedarthritis,CIA)软骨破坏的保护作用及其机制。 方法 :建立大鼠 CIA动物模型 ,随机分为 3组 :正常对照组 ,CIA组和 α- MSH注射组 ,每组 8只。于致敏建模当天起连续腹腔注射 α- MSH或 PBS,比较各组大鼠组织病理学及 X线放射学表现。收集 CIA组牛 型胶原 (b C )诱导的大鼠淋巴细胞和 L PS诱导的大鼠腹腔巨噬细胞 ,加入不同浓度的 α- MSH(10 - 1 2~ 10 - 6 mol/ L)后 ,分别培养 4 8h和 2 4 h收集上清 ,应用 EL ISA法测定 IL- 1β和 IL- 10含量 ,MTT法测定 TNF- α浓度 ,硝酸还原酶法测定一氧化氮 (NO)水平。 结果 :α- MSH可改善关节炎大鼠病灶的病理及 X线表现 ,抑制关节软骨破坏。给予α- MSH后 ,CIA大鼠腹腔巨噬细胞和淋巴细胞上清中 IL - 1β、TNF-α及 NO水平明显下降 ,IL - 10含量则明显升高。 结论 :α- MSH对关节炎大鼠软骨破坏具有抑制作用 ,其机制可能与调节细胞因子及Objective:To study the protective effect of alpha melanocyte stimulating hormone (α MSH) on cartilage destruction in collagen induced arthritis (CIA) rats. Methods: Arthritis rat model was induced by immunizing with bovine type Ⅱ collagen (bCⅡ). The rats were randomly divided into 3 groups( n =8): normal control group, CIA group and α MSH group.α MSH or PBS was administered intraperitoneally from the day of primary immunization. The histopathological and radiographic changes of rats in each group were compared. Culture supernatants of lymphocytes with α MSH and/or bCⅡand peritoneal macrophages with α MSH and/or LPS from CIA rats were harvested and analyzed respectively for IL 1β,IL 10 by ELISA. TNF α was detected by MTT assay, and NO was measured by the method of nitrate reductase. Results:α MSH markedly inhibited arthritic cartilage damage in pathology and radiography. Different concentrations of α MSH(10 -12 10 -6 mol/L) significantly suppressed the production of IL 1β and TNF α and enhanced the synthesis of IL 10 by lymphocytes and macrophages; maximal effects were obtained at a concentration of 10 -10 mol/L or 10 -8 mol/L ( P < 0.01). Conclusion: α MSH has inhibitory effect on cartilage destruction in CIA rats; the possible mechanism involves regulation of cytokines and NO levels.
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