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目的:观察《金匮要略》不同方药对肺纤维化模型早期阶段(1~14d)的影响,探讨肺纤维化早期阶段的中医基本病机与方药作用机制。方法:Wistar大鼠随机分为正常组、模型组、强的松组、栝楼薤白汤组、大黄虫丸组、肾气丸组和麦门冬汤组。除正常对照组外,其余各组均采用气管内一次性注入平阳霉素复制肺纤维化模型,造模后第2天开始灌胃用药,14d后处死动物,比较各组肺部病变程度及肺组织中肿瘤坏死因子α(TNF-α)的表达。结果:模型组肺泡炎重于正常组、栝楼薤白汤组、强的松组和麦门冬汤组、大黄虫丸组(P<0.05);肺纤维化重于正常组、栝楼薤白汤组、大黄虫丸组(P<0.05);TNF-α的表达高于正常组、栝楼薤白汤组、麦门冬汤组、强的松组和肾气丸组(P<0.05)。结论:《金匮要略》麦门冬汤、大黄虫丸及栝楼薤白汤对肺纤维化模型早期阶段肺部病变均有一定防治作用,此阶段可能以痰浊痹阻、肺阴亏虚和瘀血阻滞为基本病机;阻止肺组织中TNF-α的过度表达可能是上述方药作用机制之一。
OBJECTIVE: To observe the effect of different prescriptions of “Golden Chamber Map” on the early stage (1-14d) of pulmonary fibrosis model, and to explore the mechanism of traditional Chinese medicine and mechanism of action of traditional Chinese medicine in the early stage of pulmonary fibrosis. Methods: Wistar rats were randomly divided into the normal group, the model group, the prednisone group, the Loulouqibai Decoction group, the Dahuangchong Pill group, the Shenqiwan group and the Maimendong Decoction group. Except for the normal control group, the other groups were all treated with a single injection of Pingyangmycin in the trachea to replicate the pulmonary fibrosis model. The rats were given intragastric administration on the second day after the model was established, and animals were sacrificed 14 days later. The degree of lung lesions and lungs in each group were compared. Expression of tumor necrosis factor alpha (TNF-α) in tissues. Results: The alveolitis in the model group was heavier than that in the normal group, the Gulou Quba Decoction group, the prednisone group, the Maimendong Decoction group, and the Dahuangzhuang Pill group (P<0.05); Group, Dahuang Pill Pills group (P<0.05); The expression of TNF-α was higher than that of normal group, Qilou Loubai Decoction group, Maimendong Decoction group, Prednisone group and Shenqiwan group (P<0.05). Conclusions: “Golden Chamber” Maimendong Decoction, Dahuangchong Pill, and Loulou Qibai Decoction all have some preventive and therapeutic effects on the pulmonary lesions in the early stage of pulmonary fibrosis model. This stage may be caused by phlegm obstruction, lung yin deficiency and Blocking blood stasis is the basic pathogenesis; preventing the overexpression of TNF-α in lung tissue may be one of the mechanisms of the above prescriptions.