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目的:观察大黄素抗博莱霉素诱导大鼠肺纤维化的作用机制。方法:选用健康Wistar大鼠60只,随机分为空白组、模型组、强的松组、大黄素高、中、低剂量组,采用博莱霉素气管内吹入法,制备肺纤维化模型,于实验第29天留取标本,用免疫组化技术检测转化生长因子β1(TGF-β1)及smad3、smad7的表达。结果:大黄素中、低剂量组大鼠TGF-β1、smad3表达减弱,smad7表达明显增强。结论:大黄素的中、低剂量组能够减轻博莱霉素导致的大鼠肺纤维化程度,其作用机制与调控TGF-β1的smad3/7信号转导蛋白表达有关。
Objective: To investigate the mechanism of emodin against bleomycin-induced pulmonary fibrosis in rats. Methods: Sixty healthy Wistar rats were randomly divided into blank group, model group, prednisone group, high, medium and low dose emodin groups. Bleomycin was injected intratracheally to prepare pulmonary fibrosis model The specimens were taken on the 29th day of experiment and the expressions of TGF-β1, smad3 and smad7 were detected by immunohistochemistry. Results: The expressions of TGF-β1 and smad3 in emodin medium and low dose groups were decreased and smad7 expression was significantly increased. CONCLUSION: Emodin can alleviate the pulmonary fibrosis induced by bleomycin in medium and low dose groups, and its mechanism may be related to the regulation of Smad3 / 7 signal transduction protein of TGF-β1.