通腑泻肺法对ALI/ARDS大鼠炎症反应的调控作用

The Inhibition Effect of Tongfu Xiefei Method on Inflammatory Response in ALI/ARDS Rats

目的探讨通腑泻肺中药对ALI/ARDS大鼠炎症反应的可能作用机制。方法 27只大鼠随机分为空白组、模型组、中药组,每组9只。模型组与中药组尾静脉注射内毒素8 mg/kg,空白组大鼠静脉注射生理盐水。中药组在造模完成后给予通腑泻肺中药灌胃,每次0.01 m L/g,每日1次,共7 d,空白组与模型组予等量生理盐水灌胃。通过ELISA法检测大鼠血清及BALF中TNF-α、IL-1β、IL-6和IL-10表达,免疫组化染色及Real-Time PCR方法检测肺组织PPARγ、NF-κB p65、TLR4蛋白及其m RNA表达。结果模型组大鼠肺组织中NF-κB p65和TLR4的m RNA表达升高,PPARγ的m RNA表达下降(P<0.05),炎症因子TNF-α、IL-1β、IL-6和IL-10显著升高(P<0.05);与模型组相比,中药组NF-κB p65、TLR4的m RNA表达降低,PPARγ的m RNA表达升高(P<0.05),炎症因子显著降低(P<0.05)。结论通腑泻肺中药可以上调ALI/ARDS状态下PPARγ的表达,降低TLR4及NF-κB表达,减轻TLR4介导的炎症反应。

Objective： To explore the possible mechanism of the effect of Chinese medicine with Tongfu Xiefei function on the inflammatory response of ALI/ARDS rats. Methods： 27 rats were randomly divided into the blank group,the model group and traditional Chinese medicine group,with 9 rats in each group. Endotoxin 8 mg/kg was injected into the tail vein of the model group and TCM group. The blank group was injected with normal saline in the rats. After the model was completed,TCM group was given traditional Chinese medicine,0.01 m L/g each time,once a day,for 7 days. The blank group and the model group were given the same amount of normal saline for gastric perfusion. The expressions of TNF-α,IL-1β,IL-6 and IL-10 in serum of rats were detected by ELISA.Immunohistochemistry,Real-Time PCR were used to detect m RNA expression of PPARγ,NF-κB p65 and TLR4 in lung tissue. Results： The m RNA expression of NF-κB p65 and TLR4 in lung tissue of rats increased in the model group;the m RNA expression of PPARγ decreased（P〈0.05）. Inflammatory factors TNF-α,IL-1β,IL-6 and IL-10 increased significantly（P〈0.05）. Compared with the model group,the m RNA expression of NF-κB p65 and TLR4 decreased in Chinese medicine group. The m RNA expression PPARγ increased（P〈0.05）,and inflammatory factors decreased significantly（P〈0.05）. Conclusion： The traditional Chinese medicine with Tongfu Xiefei function can upregulate the expression of PPARγ in ALI/ARDS state,reduce the expression of TLR4 and NF-κB and the inflammatory response mediated by TLR4.