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目的观察N-乙酰基-丝氨酰-天冬氨酰-赖氨酰-脯氨酸(Ac-SDKP)能否通过调控激动型G蛋白α(Gαs)/抑制型G蛋白α(Gαi)信号对大鼠矽肺纤维化发挥保护作用。方法雄性Wistar大鼠随机分为3组(n=10):对照16周组,矽肺模型16周组,Ac-SDKP预防治疗组。采用HE染色观察肺组织病理形态的改变,Western blot检测α-平滑肌肌动蛋白(α-SMA)、Ⅰ型胶原(CollagenⅠ)、纤连蛋白(Fn)、Gαs、Gαi2、Gαi3和环磷酸腺苷(cAMP)的含量,采用免疫荧光染色检测矽肺组织α-SMA/Gαi3的共表达。结果在矽肺模型16周组,HE染色显示肺组织内出现多个细胞性结节的融合和间质纤维化的形成,并可见细胞纤维性结节的形成。免疫荧光化学染色显示在纤维化病变区域α-SMA/Gαi3共表达增强。与对照组比较,矽肺模型16周组α-SMA、CollagenⅠ、Fn、Gαi2及Gαi3的蛋白表达明显升高,Gαs和cAMP的表达明显下降;与矽肺模型16周组相比,Ac-SDKP预防治疗组肺组织病理损伤减轻,α-SMA/Gαi3共表达减少,α-SMA、CollagenⅠ、Fn、Gαi2及Gαi3的蛋白表达显著降低,Gαs和cAMP的表达明显升高。结论 Ac-SDKP能够通过调节Gαs、Gαi促进cAMP的生成对矽肺大鼠肺纤维化产生保护作用。
Objective To investigate whether N-acetyl-Seryl-Aspartyl-Lysyl-Proline (Ac-SDKP) can regulate the activation of Gαs / Gαi signaling Protective effect on silicotic fibrosis in rats. Methods Male Wistar rats were randomly divided into three groups (n = 10): the control group of 16 weeks, the silicosis model group of 16 weeks, and the group of Ac-SDKP prophylaxis and treatment. The pathological changes of lung tissue were observed by HE staining. The expressions of α-SMA, CollagenⅠ, Fn, Gαs, Gαi2, Gαi3 and A cyclic AMP (cAMP) were detected by immunofluorescence staining of silicosis α-SMA / Gαi3 co-expression. Results In the 16-week group of silicosis model, HE staining showed the formation of multiple cellular nodules and formation of interstitial fibrosis in lung tissue, and the formation of fibrous nodules. Immunofluorescence staining revealed that α-SMA / Gαi3 co-expression was enhanced in fibrotic lesions. Compared with the control group, the protein expression of α-SMA, CollagenⅠ, Fn, Gαi2 and Gαi3 in silicosis model group increased significantly and the expression of Gαs and cAMP decreased significantly in 16-week group. Ac-SDKP prophylaxis The pathological damage of lung tissue was alleviated and the co-expression of α-SMA / Gαi3 was decreased. The protein expressions of α-SMA, CollagenⅠ, Fn, Gαi2 and Gαi3 were significantly decreased, and the expressions of Gαs and cAMP were significantly increased. Conclusions Ac-SDKP can protect lung fibrosis of silicotic rats by regulating Gαs and Gαi and promoting cAMP production.