New anti-fibrotic mechanisms of n-acetyl-seryl-aspartyl-lysyl-proline in silicon dioxide-induced silicosis

Life Sciences
Ying SunXuepeng Zhang

Abstract

We previously reported that tetrapeptide N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) inhibited pulmonary inflammation and fibrosis in SiO(2)-induced silicosis. This study aimed to explore the precise mechanism involved. Rats were divided into 3 groups: 1) sham (saline), 2) silicosis+vehicle, and 3) silicosis+Ac-SDKP [800 microg/(kgd)]. SiO(2) particles or saline were administered by tracheal instillation and Ac-SDKP or vehicle (saline) via a mini-osmotic pump planted into the abdominal cavity 48 h before instillation. Animals were observed for 4 weeks. Silicotic nodule fraction (SNF) and macrophage infiltration (ED-1 positive cells) were measured by hematoxylin and eosin (H.E.) and immunohistochemical staining respectively. Collagen I and III, transforming growth factor-beta1 (TGF-beta1) proteins and monocyte chemotactic protein-1 (MCP-1) mRNA were detected by Western Blot (WB) and real-time RT-PCR respectively. In vitro, pulmonary fibroblasts were stimulated by TGF-beta1 (5 microg/ml) with or without Ac-SDKP. Phosphorylated c-Jun N-terminal Kinase (p-JNK) was detected by WB and p-JNK nuclear translocation by confocal analysis. SiO(2) significantly increased the SNF, collagen I and III proteins, TGF-beta1, MCP-1 mRNA and ma...Continue Reading

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Jan 29, 2013·Clinical and Experimental Pharmacology & Physiology·Ross G DouglasEdward D Sturrock
Aug 28, 2012·International Immunopharmacology·Hechang TanNiansheng Yang
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