映山红总黄酮的镇痛作用机制

The Analgesic Mechanism of Total Flavone of Rhododendron

目的:研究映山红总黄酮(total flavone of rhododendron,TFR)的镇痛作用机制。方法:在热板反应模型上,观察用药后小鼠舔足潜伏期的变化;采用Griess法和紫外分光光度法测定NO和PGE2的含量;逆转录-聚合酶链反应(reverse transcription-polymerase chain reaction,RT-PCR)观察TFR对诱导型一氧化氮合酶(inducible nitri-coxide synthase,iNOS)mRNA表达水平的影响。结果:TFR100、200 mg/kg可显著延长小鼠热板舔足反应潜伏期。TFR 100 mg/kg能升高小鼠血清中NO的含量,TFR200 mg/kg不仅升高脑组织中NO的含量而且增强脑组织中iN-OS mRNA的表达。TFR50、100和200 mg/kg ig可明显降低小鼠脑组织PGE2含量,200 mg/kg组可降低血清中PGE2含量。结论:TFR的镇痛作用与促进NO释放及增强iNOS mRNA的表达及抑制PGE2合成有关。

Objective ： To study the analgesic mechanisms of total flavone of rhododendmn （TFR）. Methods ： On hot-plate test in mice, the changes of the latencies of licking paws were observed after drug administration. Meanwhile, the contents of nitric oxide （NO） and prostaglandin E2 （PGE2 ） in the mice serum and cereburum were measured by Griss reaction and spectrophotomtry methods, respectively. The expression of inducible nitricoxide synthase （iNOS） in mices was detected by the reverse transcription -porymerse chain reaction （RT-PCR） technique. Results： TFR 100, 200 mg/kg ig remarkably prolonged the latencies of licking paws in mice. 100 mg/kg TFR ig significantly increased the mice serum NO content, and 200 mg/kg TFR ig markedly increased the NO content as well as promoted the iNOS mRNA expression in mice cerebrum. TFR 50,100,200 mg/kg ig significantly reduced the contents of PGE2 in mice cerebrum and 200 mg/kg TFR ig remarkably reduced the PGE2 contents in mice serum. Conclusion ： Analgesic effects of TFR may be related to promoting the release of NO and increasing expression the of iNOS as well as inhibiting the production of PGE2.