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[Antifibrotic effects of N-acetyl-seryl-aspartyl-lysyl-proline mediated by the regulation of MCP-1 and ED-1 expression on rats with silicosis].

OBJECTIVE
To investigate whether the effect of N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP) on macrophage infiltration was involved in AcSDKP's antifibrotic effect on the rats with silicosis.


METHODS
Rats were intratracheally instilled with silica as silicotic models in the experiment. Wistar rats were divided into 6 groups randomly: control 1, control 2, silicotic model 1, silicotic model 2, anti-fibrosis treatment of AcSDKP, Preventing fibrosis treatment of AcSDKP. Lung fibrosis in morphology was observed by H.E staining. Collage content was detected by Hydroxyproline assy. The expressions of MCP-1 and ED-1 in lung were observed by immunohistochemistry.


RESULTS
In anti-fibrosis treatment of AcSDKP group, area of of silicosis nodules decreased to 84.28% and 67.93%, content of hydroxyproline decreased to 70.89% and 58.18%, protein expression of MCP-1 decreased to 82.3% and 84.1%, cell numbers of MCP-1 decreased to 67.4% and 72.5%, protein expression of ED-1 decreased to 78.7% and 79.3%, cell numbers of ED-1 decreased to 54.4% and 66.8%. In Preventing fibrosis treatment of AcSDKP group, area of silicosis nodules decreased to 61.13%, content of hydroxyproline decreased to 60.27%, protein expression and cell numbers of MCP-1 decreased to 85.2% and 86.3%, protein expression and cell numbers of ED-1 decreased to 87.2% and 74.9%.


CONCLUSION
AcSDKP can decrease and reverse pulmonary fibrosis in rats with silicosis which may be mediated in part by inhibition of the infiltration and aggregation of macrophage and the severity of silicotic alveolitis.