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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。
Dynamic observation of TGP (50mg · kg-1 · d-1, ig × 27d) on the proliferation of ConA in splenic lymphocytes of adjuvant arthritis (AA) rats showed that TGP The d14,21 and d28 low card proliferation reaction returned to normal. The recombinant cell culture system was established by adherent method to purify card lymphocytes (A-), and then adding 2.5% homologous rat peritoneal macrophages (PMφ). The results showed that PMΦ in AA group could inhibit the proliferation of normal cells and A-cells in AA group, whereas PMΦ in TGF-treated AA group restored the ConA response, indicating that PMΦ is a target cell for TGP treatment . The effect of TGP on PGE2 production in AA rats was dynamically observed by radioimmunoassay. It was found that TGP could restore normal levels of PGE2 produced by d7, 14, 21 and d28 in AA rats. Correlation analysis between PGE2 and ConA showed that r = -0.55 (P> 0.05), suggesting that PMΦ could inhibit the proliferation of ConA in vitro and that other factors besides PGE2 were involved.