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目的研究N-乙酰基-丝氨酰-天门冬酰-赖氨酰-脯氨酸(AcSDKP)对矽肺模型大鼠肺内肌成纤维细胞分化的调节作用。方法采用非暴露式气管SiO2(50 g.L-1)灌注法复制大鼠矽肺模型,60只Wistar大鼠随机分为对照4 wk组、对照8 wk组、模型4 wk组、模型8 wk组、AcSDKP治疗组(塑模4 wk后给予AcSDKP 800μg.kg-1至8 wk)和AcSDKP预防治疗组(先给予AcSDKP 800μg.kg-1.d-1,48 h后制模,维持治疗至8 wk),每组10只。羟脯氨酸测量法定量分析肺组织中总胶原蛋白的含量,免疫组织化学法、Western blot检测肺组织内血清反应因子(SRF)、α-平滑肌肌动蛋白(α-SMA)、Ⅰ型和Ⅲ型胶原的表达。结果与同时点对照组相比,模型组大鼠肺组织内胶原含量和SRF、α-SMA、Ⅰ型和Ⅲ型胶原蛋白表达均增加(P<0.05)。分别与模型4 wk和8 wk组相比,AcSDKP治疗组和预防治疗组大鼠肺组织内胶原含量和SRF、α-SMA以及Ⅰ型、Ⅲ型胶原蛋白表达均明显降低(P<0.05)。结论 AcSDKP可能通过抑制矽肺大鼠肺内肌成纤维细胞的分化,减少其胶原的合成与分泌,进而发挥抗矽肺纤维化的作用。
Objective To investigate the regulatory effect of N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP) on pulmonary myofibroblasts differentiation in silicotic rat model. Methods Silicosis model was induced by non-exposed tracheal SiO2 (50 gL-1) perfusion in rats. Sixty Wistar rats were randomly divided into 4 wk control group, 8 wk control group, 4 wk model group, 8 wk model group, AcSDKP (AcSDKP 800μg.kg-1 to 8 wk after 4 weeks) and AcSDKP prophylaxis treatment group (800μg.kg-1.d-1 and 48 hours after AcSDKP was first given and maintained for 8 weeks) , Each group of 10. The content of total collagen in lung tissue was measured by hydroxyproline method. The expressions of serum reactive protein (SRF), α-smooth muscle actin (α-SMA), type Ⅰ and Type Ⅲ collagen expression. Results Compared with the control group at the same time point, the content of collagen and the expression of SRF, α-SMA, type Ⅰ and type Ⅲ collagen in the model group were all increased (P <0.05). Compared with model 4 wk and 8 wk groups, the content of collagen and the expression of SRF, α-SMA and type Ⅰ and type Ⅲ collagen in AcSDKP group and prophylaxis group were significantly decreased (P <0.05). Conclusion AcSDKP may play an important role in the prevention of silicosis by inhibiting the differentiation of pulmonary fibroblasts in silicosis in rats and reducing the synthesis and secretion of collagen.