白芍总甙对大鼠腹腔巨噬细胞产生前列腺素E_2的作用及部分机制研究

Effect of total glucosides of paeony on prostaglandin E_2 derived from peritoneal macrophapes and its sectional mechanism in rats

白芍总甙（ＴＧＰ，０．０１～１００ｍｇ·Ｌ－１）对亚适浓度Ａ２３１８７（０．１μｍｏｌ·Ｌ－１）激活的大鼠腹腔巨噬细胞（ＰＭΦ）产生的前列腺素Ｅ２（ＰＧＥ２）呈现低浓度促进和高浓度抑制的双向调节作用。而ＴＧＰ对最适浓度Ａ２３１８７（１μｍｏｌ·Ｌ－１）激活的ＰＭΦ产生的ＰＧＥ２呈浓度依赖性的抑制作用，其ＩＣ５０为１６．７ｍｇ·Ｌ－１。在整体模型上，ＴＧＰ（５０ｍｇ·ｋｇ－１×１０ｄ）能使佐剂性关节炎（ＡＡ）大鼠ＰＭΦ产生过高的ＰＧＥ２恢复正常水平。采用Ｆｕｒａ－２／ＡＭ荧光法测定ＴＧＰ对Ａ２３１８７（１μｍｏｌ·Ｌ－１）诱导正常大鼠ＰＭΦ胞内游离钙离子浓度［Ｃａ２＋］ｉ，发现ＴＧＰ（≤１０ｍｇ·Ｌ－１）对ＰＭΦ［Ｃａ２＋］ｉ无明显影响，而ＴＧＰ在（１０～１００ｍｇ·Ｌ－１）时，对ＰＭΦ［Ｃａ２＋］ｉ有一定抑制作用。提示高浓度ＴＧＰ对ＰＧＥ２的负向调节作用可能与抑制细胞内钙有关。

At the suboptimal concentration of calcimycin(A23187, 0.1μmol· L-1),the production of PGE2 was bidirectionly regulated by TGP(0.01～100 mg·L-1)with a concentration-dependent manner. In same range of the concentration of TGP,however, the amount of PGE2 from PMΦStimulated by optimal concentration of A23187(1 μmol· L-1)was inhibited with a dosedependent manner. On the 28th day in adjuvant arthritis rsts.the elevated PGE2 was restored by administration of TGP(50 mg · kg-1). Using Fura-2 fluoresence technique,it was found that the intracellular calcium ion concentration of PMΦ in normal rsts,which was stimulated by A23187(1 μmol · L-1) was inhibited by higher concentration of TGP(10～100 mg· L-1) no significant effect was found under the concentration of TGP(1 mg· L-1). The result suggest that the negative modulation of higher concentration of TGP on PGE2 production of PMΦ might be related to inhibiting intracellular calcium.