OBJECTIVE: To investigate the effect of N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP) on the collagen synthesis and expression in lung of rats with silicosis. METHODS: Rats were divided into 6 groups randomly, 10 rats in each group: Control 1 of silicotic model: each rat was intratracheally instilled with 1 ml normal sodium and was killed at the fourth week; Control 2 of silicotic model: each rat was intratracheally instilled with 1 ml normal sodium and was killed at the eighth week; Silicotic model 1: each rat was intratracheally instilled with 1 ml silica suspension and was killed at the fourth week; Silicotic model 2: each rat was intratracheally instilled with 1 ml silica suspension and was killed at the eighth week; Anti-fibrosis treatment of AcSDKP: after each rat was intratracheally instilled with 1 ml silica suspension for 4 weeks, AcSDKP 800 microg/(kgxd) was administered into every rat and rats were killed at the eighth week; Preventing fibrosis treatment of AcSDKP: after AcSDKP 800 microg/(kgxd) was administered into every rat for 48 hours, each rat was intratracheally instilled with 1 ml silica suspension and rats were killed at the eighth week. Lung fibrosis in morphology was observed by HE and VG staining. Collagen content was detected by hydroxyproline assay. The expression of type I and III collagen was evaluated by western blot. RESULTS: Compared with those of silicotic model 1 and silicotic model 2 group, in anti-fibrosis treatment of AcSDKP group, the area of silicosis nodules decreased to 84.28% and 67.93%, the content of hydroxyproline decreased to 70.89% and 58.18%, the expression of type I collagen decreased to 71.08% and 58.13%, and expression of type III collagen decreased to 80.13% and 70.70%. Compared with those of silicotic model 2 group, in preventing fibrosis treatment of AcSDKP group, area of silicosis nodules decreased to 61.13%, content of hydroxyproline decreased to 60.27%, and expression of type I and type III collagen decreased to 40.13% and 65.77%. CONCLUSION: AcSDKP could obviously inhibit the synthesis and expression of collagen in lung of rats with silicosis, which is possibly related with anti-fibrosis effect of AcSDKP.
OBJECTIVE: To investigate the effect of N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP) on the collagen synthesis and expression in lung of rats with silicosis. METHODS:Rats were divided into 6 groups randomly, 10 rats in each group: Control 1 of silicotic model: each rat was intratracheally instilled with 1 ml normal sodium and was killed at the fourth week; Control 2 of silicotic model: each rat was intratracheally instilled with 1 ml normal sodium and was killed at the eighth week; Silicotic model 1: each rat was intratracheally instilled with 1 ml silica suspension and was killed at the fourth week; Silicotic model 2: each rat was intratracheally instilled with 1 ml silica suspension and was killed at the eighth week; Anti-fibrosis treatment of AcSDKP: after each rat was intratracheally instilled with 1 ml silica suspension for 4 weeks, AcSDKP 800 microg/(kgxd) was administered into every rat and rats were killed at the eighth week; Preventing fibrosis treatment of AcSDKP: after AcSDKP 800 microg/(kgxd) was administered into every rat for 48 hours, each rat was intratracheally instilled with 1 ml silica suspension and rats were killed at the eighth week. Lung fibrosis in morphology was observed by HE and VG staining. Collagen content was detected by hydroxyproline assay. The expression of type I and III collagen was evaluated by western blot. RESULTS: Compared with those of silicotic model 1 and silicotic model 2 group, in anti-fibrosis treatment of AcSDKP group, the area of silicosis nodules decreased to 84.28% and 67.93%, the content of hydroxyproline decreased to 70.89% and 58.18%, the expression of type I collagen decreased to 71.08% and 58.13%, and expression of type III collagen decreased to 80.13% and 70.70%. Compared with those of silicotic model 2 group, in preventing fibrosis treatment of AcSDKP group, area of silicosis nodules decreased to 61.13%, content of hydroxyproline decreased to 60.27%, and expression of type I and type III collagen decreased to 40.13% and 65.77%. CONCLUSION: AcSDKP could obviously inhibit the synthesis and expression of collagen in lung of rats with silicosis, which is possibly related with anti-fibrosis effect of AcSDKP.