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目的:研究萆薢除痹汤降尿酸、抗炎及镇痛作用,并探讨其作用机制。方法:将雄性昆明小鼠32只,随机分为正常组、模型组、萆薢除痹汤组(20.9 g·kg-1给药)、别嘌呤醇组(40 mg·kg-1),每组8只,除正常组外,其他各组采用氧嗪酸钾300 mg·kg-1ip建立高尿酸血症模型,每天ig给药1次,连续7 d,试剂盒检测小鼠血清尿酸(SUA),黄嘌呤氧化酶(XOD)水平,观察萆薢除痹汤降尿酸作用及可能的降尿酸机制;另取两组雄性昆明种小鼠30只,随机分为模型组、萆薢除痹汤组(20.9g·kg-1)、别嘌呤醇组(40 mg·kg-1),每组10只,每天ig给药1次,连续3 d,分别采用冰乙酸致扭体法观察萆薢除痹汤镇痛作用、采用二甲苯致耳肿胀法观察萆薢除痹汤抗炎作用;雄性昆明种小鼠32只,随机分为正常组、模型组、萆薢除痹汤组(20 g·kg-1)、吲哚美辛组(2 mg·kg-1),每组8只,每天ig给药1次,连续6 d,通过关节腔注射尿酸盐结晶(MSU)建立急性痛风性关节炎(AGA)模型,并检测白细胞介素-1β(IL-1β),肿瘤坏死因子-α(TNF-α)水平,分析其抗炎作用及可能的机制。结果:与正常组比较,模型组SUA和XOD水平明显升高(P<0.01),IL-1β,TNF-α含量明显升高(P<0.01);与模型组比较,萆薢除痹汤能够显著降低SUA和XOD水平(P<0.05),明显降低小鼠初次扭体时间(P<0.05)和扭体次数(P<0.05),明显减轻小鼠耳肿胀程度(P<0.05),明显降低造模后24 h小鼠的踝关节肿胀度(P<0.05)和IL-1β,TNF-α(P<0.01)的表达。结论:萆薢除痹汤具有明显降低小鼠SUA作用,其降尿酸机制可能是抑制XOD的表达;萆薢除痹汤还具有抗炎镇痛作用,其抗炎作用机制可能是与IL-1β,TNF-α的含量相关。
Objective: To study the effects of Dihuang Decoction on uric acid, anti-inflammatory and analgesic effects and its mechanism of action. Methods: Thirty-two male Kunming mice were randomly divided into four groups: normal group, model group, Qiyabebi Decoction group (20.9 g · kg -1), allopurinol group (40 mg · kg -1) 8, except for the normal group, all the other groups were given ouabain 300 mg · kg-1 ip to establish hyperuricemia model, once a day for 7 days, the kit was used to detect serum uric acid (SUA) , Xanthine oxidase (XOD) were measured. The uric acid and the uric acid-lowering mechanism were observed in addition to Bi-Bu decoction. Thirty male Kunming mice were randomly divided into model group, g · kg-1), allopurinol group (40 mg · kg-1), 10 rats in each group were given ig once a day for 3 consecutive days. The mice were randomly divided into normal group (n = 20), model group (20 g · kg-1) and indole (2 mg · kg-1), 8 rats in each group, once a day for 6 days. Acute gouty arthritis (AGA) model was established by intra-articular injection of urate crystals (MSU) Interleukin-1β (IL-1β) and tumor necrosis factor were detected (TNF-α) levels, analysis of its anti-inflammatory effects and possible mechanisms. Results: Compared with the normal group, the levels of SUA and XOD in the model group were significantly increased (P <0.01) and the levels of IL-1β and TNF-α in the model group were significantly increased (P <0.01). Compared with the model group, Reduce the level of SUA and XOD (P <0.05), significantly reduce the time of first writhing (P <0.05) and the number of writhing (P <0.05), and significantly reduce the degree of ear edema (P <0.05) The ankle swelling (P <0.05) and the expression of IL-1β and TNF-α (P <0.01) in mice at 24 h after the model were made. Conclusion: Except that Bi-Tang can significantly reduce the effect of SUA in mice, the mechanism of its uric acid-lowering may be to inhibit the expression of XOD. It also has the anti-inflammatory and analgesic effects in addition to Bi-wei, and its anti-inflammatory mechanism may be related to IL-1β, -α content.