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作 者:李俊[1] 汤晓林[1] 陈敏珠[1] 徐叔云[1]
机构地区:[1]安徽医科大学临床药理研究所
出 处:《中国药理学通报》1995年第6期475-478,共4页Chinese Pharmacological Bulletin
摘 要:动态观察白芍总甙(TGP,50mg·kg-1·d-1,ig×27d)对佐剂性关节炎(AA)大鼠脾细胞刀豆球蛋白A(ConA)增殖反应发现,TGP能使d14,21与d28低下牌细胞增殖反应恢复正常。采用贴壁法纯化牌淋巴细胞(A-),再回加2.5%的同系大鼠的腹腔巨噬细胞(PMφ)建立重组细胞培养系统。结果发现,AA组的PMφ能抑制正常和AA组A-细胞的ConA增殖反应,而TGF治疗的AA组的PMφ使上述培养的ConA反应恢复正常,提示PMφ是TGP发挥治疗作用的一种靶细胞。采用放免法,动态观察TGP对AA大鼠产生PGE2的影响,发现TGP能使AA鼠d7、14、21与d28产生过高的PGE2均恢复到正常水平。PGE2与ConA反应经相关性分析,发现r=-0.55(P>0.05),提示AA大鼠PMφ对ConA增殖反应的抑制作用,除PGE2外还有其它因子参与。Immunoregulatory mechamisms of total glucosides of paeony(TGP)in adjuvant arthritic(AA)rats were studied.The results showed mat lower ConA-induced proliferative responses Of splenocytes,on the 14 th,21 th,and 28 th day respectively,were restored in AA rats treated with TGP(50 mg·kg-1 in X27d).By reconstituted culture,the diminished ConA-induced proliferative responses were found when 2.5% peritomeal macrophages(PMφ)from AA rats were added in the culture of Mφ-depleted splenocytes from AA rats of normal rats.At the same concentration of PMφ from AA rats administrated with TGP(50mg·kg-1·d-1ig×7d),however,the remarkable recovery of the diminished ConA-induced proliferative responses was observed,showing the regulatory actions of TGP in AA rats might be mediated via Mφ.The results also showed that elevated prostaglandin E2(PGE2) released from PMφ,on the 7th,14th,21th and 28th day respectively, were restored in the AA rats (50 mg·kg-1·d-1X27d).Analyses of PGE2and ConA-induced responses in AA rats by linear corelation, the corelated coefficient was found to be-0.55(P>0.05),indicating that the recovery of elevated PGE2 might be one of the mechanisms of TGP,by which the diminished ConA-induced responses of splenocytes were restored in AA rats.
分 类 号:R282.710.5[医药卫生—中药学] R965.1[医药卫生—中医学]
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