Ac-SDKP inhibits silicosis fibrosis in rats by regulating Gαs/Gαi signaling / 西安交通大学学报(医学版)

ABSTRACT

ABSTRACTObjective To observe whether N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP)can inhibit rat silicotic fibrosis by regulating stimulatory G proteinα(Gαs)/inhibitory G proteinα(Gαi)signal.Methods Male Wistar rats were randomly divided into three groups (n=1 0 )control 1 6-w group,silicosis 1 6-w group,and Ac-SDKP pre-treatment group.The pathological changes of the lung tissue was observed by HE staining;the expressions ofα-smooth muscle actin (α-SMA),Collagen Ⅰ,fibronectin (Fn),Gαs,Gαi2 ,Gαi3 and cAMP were detected by Western blot.Immunofluorescence was performed on lung tissue sections to detect the coexpression ofα-SMA/Gαi3 . Results Within silicosis 16-w group,HE staining showed that the silicotic nodule volume increased,nodule fusion and the formation of interstitial fibrosis could be seen,and cell fibrous nodules were visible.Immunofluorescence staining showed the enhanced coexpression ofα-SMA/Gαi3 in fibrosis area.Compared with those in control group, the expressions ofα-SMA,Collagen Ⅰ,Fn,Gαi2 and Gαi3 significantly increased in silicosis 1 6-w group,but the expressions of Gαs and cAMP decreased.Compared with silicosis 1 6-w group,Ac-SDKP pre-treatment group had alleviated lung injury and decreased coexpression ofα-SMA/Gαi3 .The expressions ofα-SMA,Collagen Ⅰ,Fn,Gαi2 and Gαi3 protein significantly decreased in Ac-SDKP pre-treatment group,while the expressions of Gαs and cAMP increased obviously.Conclusion Ac-SDKP can regulate the expressions of Gαs and Gαi and promote the formation of cAMP,thus playing an effective role against silicotic fibrosis.