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对吴茱萸水提物在胃寒证小鼠模型上镇痛作用的药效剂量范围及机制进行初步研究。制备胃寒证小鼠模型,采用经典的小鼠热板法,灌胃不同剂量吴茱萸水提物,观察其镇痛及伴随毒副作用,检测血清ALT,AST,PGE2,NO,NOS,MDA,SOD,GSH,GSH-Px,BUN,CR及肝脏ALT,AST;并通过相关的毒性反应积分表,记录小鼠的伴随毒性症状。吴茱萸水提物在药后30 min有明显的镇痛作用,60 min达到峰效应,呈现一定的“量-效”和“时-效”关系,血中和肝内ALT和AST水平升高,血中PGE2,MDA,NO,NOS水平的增高,SOD,GSH,GSH-Px水平下降,BUN,CR水平无明显变化,肝体比值增加,肾体比值无明显变化。吴茱萸水提物发挥镇痛效应的机制与抑制疼痛介质释放、过氧化损伤及NO损伤有关;在发挥镇痛效果的同时还会伴随着对肝脏产生一定的毒性,毒性机制主要为氧化损伤,呈现与肝毒性损伤相并行的“量-时-毒”关系。
Efficacy of Evodia rutaecarpa water extract in gastric cold syndrome mouse model of analgesic effect of dose range and mechanism of preliminary study. The mouse model of gastric cold syndrome was established. The classic mouse hot-plate method was used to gavage the aqueous extract of Evodia rutaecarpa. The analgesic and side effects were observed. The contents of ALT, AST, PGE2, NO, NOS, MDA and SOD , GSH, GSH-Px, BUN, CR and liver ALT, AST. The related toxicity symptoms were recorded in the relevant toxicological reaction integral tables. Fructus Evodiae water extract had obvious analgesic effect at 30 min and reached the peak effect at 60 min, showing a certain relationship between “quantity-effect” and “time-effect”, blood and liver ALT and AST The levels of PGE2, MDA, NO and NOS in blood increased, the levels of SOD, GSH and GSH-Px decreased, while the levels of BUN and CR had no significant changes. Evodia water extract play an analgesic effect mechanism and inhibit the release of pain mediators, peroxide damage and NO damage; in the exertion of analgesic effect also accompanied by a certain degree of toxicity to the liver, the main toxic mechanism of oxidative damage, showing A “quantity-time-toxic” relationship in parallel with hepatotoxic injury.