Abstract
Oxymatrine, one kind of alkaloids extracted from Sophora flavescens Ait, has been demonstrated to attenuate bleomycin-induced lung fibrosis. The mechanisms of this action are poorly known. This study aimed to use proteomics to provide new insights into the mechanisms of the pharmacological effects. Proteins from murine lung fibroblasts exposed to oxymatrine were separated by two-dimensional electrophoresis. Differentially expressed proteins were identified using mass spectrometry. A two-dimensional cell migration assay was used to study the effects of oxymatrine on fibroblast migration activity. Among these detectable protein spots on the 2-DE gel 9 protein, spots were signii¬cantly altered in oxymatrine treated cells. 5 proteins were successfully identii¬ed. All were down-regulated by oxymatrine. Mass spectrometer analysis indicated that one of these proteins is a metabolic enzyme, while others are related to cytoskeleton or involved in cellular transcription and translation. The attenuated expressions of mRNA and protein of the cytoskeleton-related protein, HSP27, were confirmed by Western blotting and RT-PCR analysis. Besides these, the migration activity of fibroblast was reduced by oxymatrine. It is suggested that regulation of HSP27 expression by oxymatrine is associated with its inhibitory effects on motility of lung fibroblasts, which contributes to the protective action of this drug against lung fibrosis. Key words: Oxymatrine, fibroblasts, proteomics, heat shock protein 27, motility.
Highlights
Pulmonary fibrosis is characterized by an absolute increase of collagen-rich extracellular matrix
Mass spectrometer analysis indicated that one of these proteins is a metabolic enzyme, while others are related to cytoskeleton or involved in cellular transcription and translation
It is suggested that regulation of heat shock protein 27 (HSP27) expression by oxymatrine is associated with its inhibitory effects on motility of lung fibroblasts, which contributes to the protective action of this drug against lung fibrosis
Summary
Pulmonary fibrosis is characterized by an absolute increase of collagen-rich extracellular matrix. The accumulation of extracellular matrix, damage of alveolar wall and loss of functional capillary units can lead to respiratory failure within a few years after diagnostic confirmation. Specific treatments for fibrotic lung diseases are not yet available. Novel therapeutic agents with improved efficacy are needed (Datta et al, 2011; Gross and Hunninghake, 2001). It is likely that multiple abnormalities in a myriad of biological pathways affect inflammation and wound repair, including matrix regulation, epithelial reconstitution, the coagulation cascade, neovascularization and antioxidant pathways. Current research results indicated that fibroblast activetion lead to progressive fibrosis. Regulation of fibroblasts should be an important therapeutic strategy (Datta et al, 2011)
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