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[目的]观察N-乙酰基-丝氨酰-天门冬酰-赖氨酰-脯氨酸(AcSDKP)对大鼠矽肺纤维化肺组织中胶原含量、转化生长因子-β1(TGF-β1)、Smad2/3和Smad 7表达的调节,探讨AcSDKP拮抗矽肺纤维化的作用机制。[方法]选用非暴露式气管灌注法制作大鼠矽肺模型,并给予AcSDKP,采用羟脯氨酸测量法和Western-blot法定量分析肺组织中胶原蛋白的含量。Western-blot法检测肺组织内TGF-β1、phospho-Smad2/3及Smad7蛋白的表达。[结果]AcSDKP治疗组胶原含量和I型、III型胶原的表达低于相对应的矽肺模型组。与相应的对照组相比,矽肺模型组大鼠肺组织内TGF-β1、phospho-Smad2/3蛋白表达均增加,而Smad7蛋白表达减弱。与相应矽肺模型组相比,给予AcSDKP后,大鼠肺组织内TGF-β1、phospho-Smad2/3蛋白表达表达均明显降低。而Smad7蛋白表达增强。[结论]AcSDKP可能是通过对TGF-β1介导Smad通路调节而发挥抗矽肺纤维化的作用。
[Objective] To observe the effects of AcSDKP on collagen, transforming growth factor-β1 (TGF-β1) Smad2 / 3 and Smad7 expression regulation, to explore the mechanism of AcSDKP antagonistic silicosis of fibrosis. [Methods] Non-exposed tracheal perfusion method was used to make rat silicosis model and AcSDKP was given. The content of collagen in lung tissue was quantitatively analyzed by hydroxyproline and Western-blot. Western-blot was used to detect the expression of TGF-β1, phospho-Smad2 / 3 and Smad7 in lung tissue. [Results] The expression of collagen and type I and type III collagen in AcSDKP treated group were lower than those in corresponding silicosis model group. Compared with the corresponding control group, the expression of TGF-β1 and phospho-Smad2 / 3 in lung tissue of silicotic model group increased, while the expression of Smad7 protein decreased in silicosis model group. Compared with the corresponding silicosis model group, the expression of TGF-β1 and phospho-Smad2 / 3 protein in lung tissue of rats were significantly decreased after AcSDKP administration. While Smad7 protein expression increased. [Conclusion] AcSDKP may play an anti-silicotic role in fibrosis through the regulation of TGF-β1-mediated Smad pathway.