论文部分内容阅读
目的:研究黄芪总甙(astragalosides,AST)的镇痛作用及其作用机制。方法:采用小鼠福尔马林致痛模型,对痛反应进行评分。通过福尔马林试验前30min皮下注射吗啡和纳络酮或福尔马林试验前20min腹腔内注射L-精氨酸和L-NAME以研究阿片肽和一氧化氮在此疼痛模型中的作用并对AST的作用与吗啡和L-NAME进行比较。结果:AST20,40和80mg/kg可显著降低小鼠福尔马林致痛后第二时相的疼痛反应(P<0.01)。AST 40mg/kg最大镇痛作用见于给药后4h(第二时相疼痛反应的抑制率为34.4％)。吗啡5mg/kg对两个时相的疼痛反应均有明显抑制作用(P<0.01),此抑制作用能被纳络酮2mg/kg拮抗(P<0.01),而AST的镇痛作用不受纳络酮影响。L-精氨酸(400或800mg/kg)可部分抑制AST的作用(P<0.01)。结论:AST所具有的镇痛作用不是通过内源性阿片肽系统介导,而可能与抑制NO等参与疼痛反应的炎症介质的生成有关。
Objective: To study the analgesic effect of astragalosides (AST) and its mechanism of action. METHODS: A mouse formalin induced pain model was used to score pain responses. The role of opiate peptides and nitric oxide in this pain model was studied by intraperitoneal injection of L-arginine and L-NAME 20 min before morphine and naloxone injection or formalin test 30 min before the formalin test. The effect of AST was compared with morphine and L-NAME. RESULTS: AST20, 40 and 80 mg/kg significantly reduced the pain response after formalin induced pain in the second phase (P<0.01). The AST 40 mg/kg maximal analgesic effect was seen 4 h after administration (the inhibition rate of the second phase pain response was 34.4%). Morphine 5 mg/kg significantly inhibited the pain responses of both phases (P<0.01). This inhibitory effect was antagonized by naloxone 2 mg/kg (P<0.01), whereas the analgesic effect of AST was not affected. Effect of ketones. L-arginine (400 or 800 mg/kg) partially inhibited the effects of AST (P<0.01). Conclusion: The analgesic effect of AST is not mediated by endogenous opioid peptide system, but may be related to the inhibition of NO and other inflammatory mediators involved in the pain reaction.