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Página 1 a partir de 27 resultados
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
[Antifibrotic effects of N-acetyl-seryl-aspartyl-lysyl-proline mediated by the regulation of MCP-1 and ED-1 expression on rats with silicosis].
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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
[Comparative proteomic analysis on anti-fibrotic effect of N-acetyl-seryl-aspartyl-lysyl-proline in rats with silicosis].
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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
[Effect of N-acetyl-seryl-aspartyl-lysyl-proline on regulation of expression of ras-raf-ERK1/2 signal transduction pathway in lung of rats with silicosis].
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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
[Antifibrotic effects of N-acetyl-seryl-aspartyl-lysyl-proline mediated by regulation of transforming growth factor beta and connective tissue growth factor expression on rats with silicosis].
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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
[Regulating effect of N-acetyl-seryl-aspartyl-lysyl-proline on activation of c-jun N-terminal kinase pathway in rats with silicosis].
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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
Acetylated α-Tubulin Regulated by N-Acetyl-Seryl-Aspartyl-Lysyl-Proline(Ac-SDKP) Exerts the Anti-fibrotic Effect in Rat Lung Fibrosis Induced by Silica.
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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
[Anti-fibrotic role of AcSDKP through inhibition of P38MAPK pathway activity mediated transforming growth beta receptors in rat with silicosis].
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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
Protective effect of Ac-SDKP on alveolar epithelial cells through inhibition of EMT via TGF-β1/ROCK1 pathway in silicosis in rat.
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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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