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机构地区:[1]安徽医科大学,临床药理研究所,抗炎免疫药理学省部共建教育部重点实验室,安徽省中药研究与开发重点实验室,安徽合肥230032 [2]安徽医科大学附属省立医院药剂科,安徽合肥230001
出 处:《中国药理学通报》2009年第1期44-47,共4页Chinese Pharmacological Bulletin
基 金:国家自然科学基金资助项目(No30572356);安徽省科技攻关计划项目(No06013133B);安徽省教育厅自然科学基金资助项目(No2006KJ334B)
摘 要:目的探讨rIL-1α对佐剂性关节炎(AA)大鼠滑膜细胞功能的影响及木瓜苷(GCS)的作用。方法采用弗氏完全佐剂(FCA)诱导大鼠AA模型,分离培养大鼠成纤维样滑膜细胞(FLS),用MTT法检测FLS的增殖能力,放射免疫法(RIA)测定FLS产生PGE2和cAMP的水平。结果在10μg·L-1的rIL-1α(1、2、4、8、24h)体外刺激下,AA大鼠FLS产生的PGE,水平升高,cAMP水平在1~8h升高,24h反而下降。GCS(100、50、25、12.5mg·L-1)体外给药可不同程度的抑制FLS的增殖反应和PGE2的产生,升高cAMP水平。结论rIL-1α可以促进AA大鼠FLS的增殖,降低cAMP,升高PGE2,GCS能明显逆转rIL-1α对FLS的影响。Aim To study effects Of glucosides of chaenomeles speciosa (GCS) on fibroblast-like synoviocytes (FLS) under the stimulation of recombinant rat interleukin-l-alpha (rIL-1α) and investigate the mechanism. Methods Complete Freund's adjuvant (FCA) was used to induce adjuvant arthritis (AA) in rats. The joint fibroblast-like synoviocytes (FLS) from AA rats were collected and incubated. Synoviocyte proliferation was determined by 3-(4, 5-dimethylthia- zal-2yl) 2, 5-diphenyltetrazolium bromide (MTT) as- say. Levels of PGE2 and cAMP were determined by radioimmunoassay (RIA). Results Level of PGE2 produced by FLS under the stimulation of rIL-lc~ (1,2,4, 8,2d h)was elevated. Level of cAMP produced by FLS under the stimulation of rIL-1α (1,2,4,8 h )was elevated, but reduced in 24 h. GCS (100, 50, 25, 12.5 mg · L-1 ) inhibited the proliferation and decreased the level of PGE2 and increased the level of cAMP. Conclusion GCS shows a capacity to reverse the rIL-1α stimulation on the FLS.
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