论文部分内容阅读
目的观察丹芍化纤对博来霉素致肺纤维化大鼠肺组织中TGF-β1及Smad3/7表达的影响。方法将30只SD大鼠,随机均分为对照组、模型组和治疗组;给予模型组和治疗组大鼠的气管内注射博来霉素(5 mg·kg-1)诱导肺纤维化,对照组的气管内注射等量生理盐水;次日起ig给予治疗组大鼠丹芍化纤混悬液(0.8 g·kg-1·d-1),其余两组ig给予等量生理盐水;28 d后处死,观察各组大鼠肺组织病理变化;运用免疫组化法观察肺组织中TGF-β1及Smad3/7表达的变化。结果模型组大鼠的肺系数明显增加,肺组织中胶原沉积明显,羟脯氨酸含量、TGF-β1和Smad3的表达增加,而Smad7表达下降;与模型组比较,治疗组大鼠的肺系数明显降低,肺组织中胶原沉积有所减轻,羟脯氨酸的含量、TGF-β1和Smad3蛋白的表达减少,而Smad7表达升高。结论丹芍化纤具有较好的抗大鼠肺纤维化作用,其机制可能与丹芍化纤影响TGF-β1/Smads信号转导通路、下调TGF-β1及Smad3的表达,同时上调Smad7的表达有关。
Objective To observe the effects of Danshuo chemical fiber on the expression of TGF-β1 and Smad3 / 7 in lung tissue of bleomycin-induced pulmonary fibrosis rats. Methods Thirty Sprague-Dawley rats were randomly divided into control group, model group and treatment group. Bleomycin (5 mg · kg-1) was given intratracheally to the model group and the untreated group to induce pulmonary fibrosis, In the control group, an equal volume of normal saline was injected intratracheally; the rats in the treatment group were treated with Danshen Chemical Fiber (0.8 g · kg -1 · d -1) ig at the next day, and the other two groups were given the same amount of saline; The rats were sacrificed and the pathological changes of lung tissue were observed. The expressions of TGF-β1 and Smad3 / 7 in lung tissue were observed by immunohistochemistry. Results Compared with the model group, the lung coefficient of the model group was significantly increased, and the collagen deposition in the lung tissue was obvious. The content of hydroxyproline, the expression of TGF-β1 and Smad3 increased, while the expression of Smad7 decreased. Compared with the model group, Significantly reduced the collagen deposition in the lung tissue was reduced, hydroxyproline content, TGF-β1 and Smad3 protein expression decreased, while Smad7 expression increased. Conclusion Danshen chemical fiber has good anti-pulmonary fibrosis effect in rats. The mechanism may be related to the effect of Danshen chemical fiber on TGF-β1 / Smads signal transduction pathway, down-regulating the expression of TGF-β1 and Smad3 and up-regulating the expression of Smad7.