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silicosis/proline

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Leht 1 alates 27 tulemused

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

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OBJECTIVE 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. METHODS Rats were divided into 3 groups: 1) sham (saline), 2)

[Anti-fibrotic effect of N-acetyl-seryl-aspartyl-lysyl-proline in lung of rat with silicosis].

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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
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
OBJECTIVE To perform a comparative proteomic analysis for identification of pulmonary proteins related to the progression of silicosis and anti-fibrotic effect of N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP). METHODS Bronchial instillation of SiO₂powder (for 4 or 8 weeks) was applied in rats to
OBJECTIVE to investigate the effect of N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP) on the expressions of c-Raf, ERK1/2 and TGF-β1 in the lung of rats with silicosis, thus to investigate the regulating of AcSDKP on the Ras-Raf-ERK1/2 signal transduction pathway. METHODS rats were instilled with
OBJECTIVE To investigate whether the effect of N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP) on transforming growth factor beta (TGF-beta1) and connective tissues growth factor (CTGF) was involved in AcSDKP's antifibrotic effect on the rats with silicosis. METHODS Rats were divided into 6 groups
OBJECTIVE To investigate the regulatory effect of N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP) on the activation of c-jun N-terminal kinase (JNK) signal transduction pathway and its role in silicotic fibrosis. METHODS A rat model of silicosis was developed by intratracheal instillation. Sixty rats

Treatment of experimental silicosis with antifibrotic agents.

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We tested the efficacy of 2 antifibrotic agents, the proline analogue cis-4-hydroxy-L-proline (cHyp) and the lathyrogen beta-aminopropionitrile (BAPN), on experimental silicosis in hamsters. Silica (75 mg) was instilled intratracheally, and 3 months later lung hydroxyproline content, the volume

Quantitative image analysis of lung connective tissue in murine silicosis.

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Pulmonary fibrosis is a disabling consequence of many lung diseases but is difficult to quantify. Lucifer yellow CH fluorescent dye (LY) appears to stain connective tissue matrix macromolecules selectively. Laser scanning confocal microscopy can quantify the intensity of fluorescence and determine
Silicosis is the most serious occupational disease in China. The objective of this study was to screen various proteins related to mechanisms of the pathogenesis of silicosis underlying the anti-fibrotic effect of N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) using proteomic profile analysis. We

Silicosis and fibrogenesis: fact and artifact.

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Although the pulmonary and extrapulmonary manifestations of silicosis in humans have been extensively documented, the mechanisms by which the fibrogenic effects of silica are manifested remain obscure. In this review, both in vitro and in vivo models of silicosis are discussed, with emphasis on the
OBJECTIVE To investigate the distribution and expression of transforming growth factor beta (TGF-β) receptors I and II, p38 mitogen-activated protein kinase (p38 MAPK), and type I and type III collagen in the lungs of rats with silicosis and cultured pulmonary fibroblasts, and to investigate the

Changes in free and bound amino acids in experimental silicosis.

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The amino acid composition of lung, serum and liver in silicotic rats was studied in order to assess the availability of precursors in lung for fibrogenesis. It was observed that the pool of ornithine, arginine, alanine, leucine, valine, glutamic acid, lysine, proline and glycine underwent marked
The epithelial-mesenchymal transition (EMT) is a critical stage during the development of silicosis fibrosis. In the current study, we hypothesized that the anti-fibrotic tetrapeptide, N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) may exert its anti-fibrotic effects via activation of the

Cis-4-[(18)F]fluoro-L-proline PET imaging of pulmonary fibrosis in a rabbit model.

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A fluorinated analog of proline amino acid, cis-4-[(18)F]fluoro-L-proline (FP), was tested for potential use in PET for detection and evaluation of pulmonary response to respirable crystalline silica. The purpose of the study was to determine whether PET imaging with FP is sensitive for detection of
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