白芍总甙对佐剂性生关节炎大鼠的免疫调节机制

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 mechanisms of total glucosides of paeony in adjuvant arthritic rats

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.