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本文研究了白芍总甙（ＴＧＰ）对大鼠佐剂性关节炎（ＡＡ）滑膜细胞功能以及脾淋已细胞增殖反应的影响及其作用机理。结果表明，ＴＧＰ５０ｍｇ·ｋｇ－１·ｄ－１×１０ｄｉｇ可使ＡＡ大鼠滑膜细胞过度分泌白介素１，肿癌坏死因子（ＴＮＦ）和前列腺素Ｅ２（ＰＧＥ２）的功能恢复正常，继而下调滑膜成纤维细胞的增殖；吲哚美辛２ｍｇ·ｋｇ－１·ｄ－１×１０ｄｉｇ抑制ＰＧＥ２产生，但增加ＡＡ大鼠滑膜细胞分泌白介素１与ＴＮＦ，从而促进滑膜成纤维细胞的增殖。ＴＧＰ５０ｍｇ·ｋｇ－１·ｄ－１×１０ｄｉｇ恢复ＡＡ大鼠脾细胞过低的伴刀豆球蛋白Ａ（ＣｏｎＡ）增殖反应与其下调巨噬细胞产生一氧化氮和ＰＧＥ２有关；体外实验亦证明，高浓度（０．４——６．４ｍｇ·Ｌ－１）ＴＧＰ负调节脾细胞ＣｏｎＡ增殖反应与其促进巨噬细胞产生一氧化氮和ＰＧＥ２有关。
This paper studied the effects of TGP on the synoviocyte function and the proliferation of splenocytes in rats with adjuvant arthritis (AA) and its mechanism of action. The results showed that TGP50mg·kg-1·d-1×10dig could make the synoviocytes of AA rats excessively secrete interleukin-1, and the function of tumor necrosis factor (TNF) and prostaglandin E2 (PGE2) returned to normal, and then the synovial membrane was down-regulated. Fibroblast proliferation; indomethacin 2mg·kg-1·d-1×10dig inhibited PGE2 production but increased interleukin-1 and TNF in synovial cells of AA rats, thereby promoting the proliferation of synovial fibroblasts. The recovery of concanavalin A (ConA) proliferative response of spleen cells in AA rats restored by TGP 50mg·kg-1·d-1×10dig was related to the downregulation of nitric oxide and PGE2 production by macrophages. In vitro experiments also showed that The concentration of (0.4-6.4 mg·L-1) TGP negatively regulates the proliferation of splenocytes ConA and is related to the promotion of nitric oxide and PGE2 production by macrophages.