雷公藤红素对IL-1和IL-2活性及PGE2释放的抑制作用

雷公藤红素0.1～1.0μg/ml在试管内能降低LPS诱导的小鼠腹腔巨噬细胞外和细胞内白细胞介素-1(IL-1)的活性,也能抑制ConA诱导的小鼠脾细胞产生白细胞介素-2(IL-2).动态观察表明,雷公藤红素经预处理8h和3h后已能分别抑制IL-1和IL-2的产生。此外,雷公藤红素能降低A23187刺激家兔滑膜细胞释放前列腺素E₂(PGE₂)。

INHIBITORY EFFECT OF TRIPTERINE ON ACTIVITIES OF IL-1, IL-2 AND RELEASE OF PGE2

Tripterine is one of the components isolated from Tripterygium wilfordii Hook. Previous studies demonstrated that tripterine inhibited not only humoral and cellular immune responses but also some inflammatory responses. The present investigation attempted to observe effect of the drug on productions of IL-1 from macrophages, IL- 2 from splenocytes and PGE₂ from synovial cells. The results showed that tripterine (0. 1 ～ 1.0μg/ml )significantly inhibited IL-1 activity of murine peritoneal macrophages induced by LPS. Because both intracellular and extracellular IL- 1 activities were decreased, so tripterine might be able to reduce the production and release of IL- 1. Besides, inhibiton of IL-1 production was observed when macrophages were pretreated with the drug for 8 h and 16 h. A good relationship was found between the effect and concentration of tripterine which inhibited IL-2 production from ConA-activated murine splenocytes. Kinetic study indicated that IL- 2 production was decreased when splenocytes were pretreated with the drug for 3 h, 6h and 12 h. Synovial cells obtained from rabbit knee joint were cultured successfully. A23187 was found to augment PGE₂ synthesis modestly. Tripterine significantly reduced PGE₂ release from synovial cells in a concentration dependent manner.