论文部分内容阅读
目的:探讨以消石利尿化瘀立法创制的中药复方的抗炎机制。方法:将雄性Wistar大鼠随机分为空白组、模型组、痛风定胶囊组、苯溴马隆组及中药复方高、中、低剂量组,共7组。除空白组外,其余各组均以腺嘌呤和乙胺丁醇灌胃,同时各给药组灌胃给予相应的药物;空白组和模型组给予等体积蒸馏水,连续10d。末次给药后,采用放射免疫分析法测定大鼠血清白介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)、白介素-4(IL-4)的含量。结果:中药复方中剂量组大鼠血清IL-1β含量与模型组比较,显著降低(P<0.05)。中药复方各组大鼠血清TNF-α含量均较模型组显著降低(P<0.01,P<0.05)。中药复方中剂量组大鼠血清IL-4含量与模型组比较显著升高(P<0.05)。结论:以消石利尿化瘀法创制的中药复方抗炎机制可能与降低IL-1β、TNF-α含量,从而减轻产生多种炎性介质的激活效应,进而抑制炎症的发生有关;也和升高抗炎性细胞因子IL-4的含量,进而抑制炎性细胞因子的合成有关。
Objective: To explore the anti-inflammatory mechanism of traditional Chinese medicine compound created by the legislation of pebble diuretic and blood stasis. Methods: Male Wistar rats were randomly divided into blank group, model group, Tongfengding Capsule group, benzbromarone group and traditional Chinese medicine compound high, medium and low dose groups, a total of 7 groups. Except for the blank group, the other groups were given gavage with adenine and ethambutol, while the corresponding drug was given by gavage in each administration group. The blank group and the model group were given equal volume of distilled water for 10 days. After the last administration, the levels of serum IL-1β, TNF-α and IL-4 were determined by radioimmunoassay. Results: Compared with the model group, the content of IL-1β in the middle-dose traditional Chinese medicine compound group was significantly lower (P <0.05). Compared with model group, the content of TNF-α in serum of rats of TCM compound prescription group decreased significantly (P <0.01, P <0.05). The content of IL-4 in the middle-dose traditional Chinese medicine compound group was significantly higher than that in the model group (P <0.05). Conclusion: The anti-inflammatory mechanism of traditional Chinese medicine formulated by the method of pebble diuretic and dissipating blood stasis may be related to reducing the content of IL-1β and TNF-α, thereby reducing the activation effect of producing a variety of inflammatory mediators, thereby inhibiting the occurrence of inflammation; High anti-inflammatory cytokine IL-4 content, thereby inhibiting the synthesis of inflammatory cytokines.