雷公藤多甙治疗类风湿关节炎的机理：Ⅱ.对细胞分泌PGE2的影响

本实验观察雷公藤多甙(T_2)对体外培养的正常人及类风湿性关节炎(RA)患者周围血单个核细胞(PBMC)产生前列腺素E_2(PGE_2)能力的影响,并与前列腺素抑制剂消炎痛及地塞米松的作用进行比较。结果发现,T_2可抑制PBMC在体外产生PGE_2,其抑制作用比消炎痛稍弱,但比地塞米松强。

Mechanism of treating rheumatoid arthritis with Tripterygium wilfordii hook. II. Effect on PGE2 secretion

PBMC from normal adults and patients with rheumatoid arthritis (RA) were cultured in the absence or presence of various concentrations of T2, indomethacin, dexamethasone for certain periods of time. The amounts of PGE2 in the cell-free supernatants were measured by radioimmunoassay, and a significant reduction of PGE2 production by PBMC cultured with 2-50 micrograms/ml of T2 was found. The percentages of inhibition of PGE2 production in the cultures with 2 micrograms/ml, 10 micrograms/ml and 50 micrograms/ml of T2 were 44.1 +/- 5.3%, 89.5 +/- 4.9% and 84.3 +/- 8.5% respectively. The PGE2 concentrations in the culture supernatants of RA PBMC were higher than those in the supernatants of normal PBMC, but the inhibitory effect of T2 on RA PBMC production of PGE2 was similar to that on normal PBMC. In comparison with indomethacin, the inhibitory effect of T2 on PGE2 production was less remarkable. However, T2 exhibits therapeutic effects on RA which are superior to any other non-steroid anti-inflammatory drug, suggesting that the inhibitory effect of T2 on PGE production may only be one of its therapeutic mechanisms in the treatment of patients with RA.