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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。
The concentrations of prostaglandin E2 (PGE2) produced by peritoneal macrophages (PMΦ) stimulated by A23187 (0.1 μmol·L-1) at the concentrations of TGP (0.01-100 mg · L-1) Showing two-way regulation of low concentration and high concentration inhibition. TGP inhibited PGE2 produced by PMΦ with the optimal concentration of A23187 (1μmol·L-1) in a concentration-dependent manner with an IC50 of 16.7mg · L-1. In the overall model, TGP (50 mg · kg-1 × 10d) can restore normal levels of PGE2 in PMΦ-producing rats with adjuvant arthritis (AA). The intracellular free calcium concentration [Ca2 +] i of PMΦ induced by A23187 (1μmol·L-1) in TGP (≤10mg · L-1) was determined by Fura-2 / i had no significant effect, while TGP (10 ~ 100mg · L-1), PMΦ [Ca2] i have some inhibition. Tip high concentration of TGP PGE2 negative regulation may be related to inhibition of intracellular calcium.