The effect of sesamin on airway fibrosis in vitro and in vivo

Lin, Ching Huei; Shen, Mengqi; Kao, Shung Te; Wu, Dong

doi:10.1016/j.intimp.2014.06.031

Cited by 10 publications

(9 citation statements)

References 56 publications

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“…In addition, the suppressive effects of natural compounds on airway remodeling in an animal model of bronchial asthma have been described. These compounds include kaempferol, triptolide, praeruptorin, and sesamin, which act as inhibitors of TGF-β1/Smad signaling 192021…”

Section: Introductionmentioning

confidence: 99%

Inhibitory Effects of Resveratrol on Airway Remodeling by Transforming Growth Factor-β/Smad Signaling Pathway in Chronic Asthma Model

Lee

Kim

Yoon

et al. 2017

Allergy Asthma Immunol Res

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PurposeAsthma is a chronic airway disease characterized by airway remodeling, leading to a progressive decline in lung function. Therapeutic agents that attenuate airway remodeling can complement the limited effects of traditional glucocorticoids. In this study, we investigated the effect of resveratrol on allergic airway inflammation and remodeling in a murine model of chronic bronchial asthma.MethodsPeribronchial smooth muscle thickening that developed in mice challenged with a 3-month repeated exposure to ovalbumin (OVA) was used to study airway remodeling. Oral resveratrol was administered daily during the OVA challenge. The expression of TGF-β1/Smad signaling proteins and downstream mesenchymal markers in the presence or absence of resveratrol was examined in bronchial epithelial cells.ResultsOVA sensitization and chronic challenge increased airway hyperresponsiveness, inflammation, goblet cell hyperplasia, α-smooth muscle actin (SMA), and collagen deposition. Resveratrol effectively suppressed OVA-induced airway inflammation and remodeling. The expression of TGF-β1/phosphorylated Smad2/3 was increased in the lung tissues of OVA-challenged mice but effectively inhibited by resveratrol. In bronchial epithelial cells, the TGF-β1-induced expression of the mesenchymal markers snail, slug, vimentin, and α-SMA was suppressed by resveratrol treatment.ConclusionsResveratrol effectively ameliorated both airway inflammation and airway structural changes in a mouse model of bronchial asthma. These effects were mediated by decreased TGF-β1 expression, in turn suppressing TGF-β1/Smad signaling and the epithelial-mesenchymal transition process. Our results demonstrate the potential benefits of resveratrol for the treatment of airway remodeling associated with bronchial asthma.

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Section: Introductionmentioning

confidence: 99%

Inhibitory Effects of Resveratrol on Airway Remodeling by Transforming Growth Factor-β/Smad Signaling Pathway in Chronic Asthma Model

Lee

Kim

Yoon

et al. 2017

Allergy Asthma Immunol Res

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“…Generally, the tested compounds are co-incubated with fibroblasts before or during the process of TGF-β1 stimulation in anti-fibrotic research in vitro 202122, aiming to reducing the transformation of myofibroblasts from fibroblasts. In this respect, RHA at 10–30 mg/L was firstly co-incubated with fibroblasts for 12 h before TGF-β1 stimulation, but unexpectedly it could not block the transformation of myofibroblasts from fibroblasts after TGF-β1 stimulation (Fig.…”

Section: Resultsmentioning

confidence: 99%

Targeted killing of myofibroblasts by biosurfactant di-rhamnolipid suggests a therapy against scar formation

Shen

Jiang

Shao

et al. 2016

Sci Rep

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Pathological myofibroblasts are often involved in skin scarring via generating contractile force and over-expressing collagen fibers, but no compound has been found to inhibit the myofibroblasts without showing severe toxicity to surrounding physiological cells. Here we report that di-rhamnolipid, a biosurfactant secreted by Pseudomonas aeruginosa, showed potent effects on scar therapy via a unique mechanism of targeted killing the myofibroblasts. In cell culture, the fibroblasts-derived myofibroblasts were more sensitive to di-rhamnolipid toxicity than fibroblasts at a concentration-dependent manner, and could be completely inhibited of their specific functions including α-SMA expression and collagen secretion/contraction. The anti-fibrotic function of di-rhamnolipid was further verified in rabbit ear hypertrophic scar models by presenting the significant reduction of scar elevation index, type I collagen fibers and α-SMA expression. In this regard, di-rhamnolipid treatment could be suggested as a therapy against skin scarring.

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“…Elevated subepithelial TGF-β is a prerequisite to collagen accumulation 26 . Airway epithelial cells challenged by airborne allergens and irritants 2728 , along with recruited eosinophils 2930 , both release TGF-β, the main pro-fibrotic cytokine 31 . Clinical studies showed elevation in TGF-β levels and subsequent collagen deposition in the airway within 48 hours of allergen exposure or methacholine-induced bronchoconstriction 32 .…”

Section: Discussionmentioning

confidence: 99%

“…TGF-β receptors on the cell surface of fibroblasts signal via Smad-3 to initiate the phenotypic change from fibroblast to myofibroblast 33 . The TGF-β induced upregulation of the cytoskeletal protein α-smooth muscle actin (α-SMA) is a direct characteristic of fibroblast activation and transformation to the myofibroblast phenotype 2331 . Interleukin-5 (IL-5) also plays a role in this pathway, stimulating the release of TGF-β by eosinophils 34 .…”

Section: Discussionmentioning

confidence: 99%

Quantification of airway fibrosis in asthma by flow cytometry

et al. 2018

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Airway fibrosis is a prominent feature of asthma, contributing to the detrimental consequences of the disease. Fibrosis in the airway is the result of collagen deposition in the reticular lamina layer of the subepithelial tissue. Myofibroblasts are the leading cell type involved with this collagen deposition. Established methods of collagen deposition quantification present various issues, most importantly their inability to quantify current collagen biosynthesis occurring in airway myofibroblasts. Here, a novel method to quantify myofibroblast collagen expression in asthmatic lungs is described. Single cell suspensions of lungs harvested from C57BL/6 mice in a standard house dust mite model of asthma were employed to establish a flow cytometric method and compare collagen production in asthmatic and non-asthmatic lungs. Cells found to be CD45 αSMA , indicative of myofibroblasts, were gated, and median fluorescence intensity of the anti-collagen-I antibody labeling the cells was calculated. Lung myofibroblasts with no, medium, or high levels of collagen-I expression were distinguished. In asthmatic animals, collagen-I levels were increased in both medium and high expressers, and the number of myofibroblasts with high collagen-I content was elevated. Our findings determined that quantification of collagen-I deposition in myofibroblastic lung cells by flow cytometry is feasible in mouse models of asthma and indicative of increased collagen-I expression by asthmatic myofibroblasts. © 2018 International Society for Advancement of Cytometry.

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The effect of sesamin on airway fibrosis in vitro and in vivo

Cited by 10 publications

References 56 publications

Inhibitory Effects of Resveratrol on Airway Remodeling by Transforming Growth Factor-β/Smad Signaling Pathway in Chronic Asthma Model

Inhibitory Effects of Resveratrol on Airway Remodeling by Transforming Growth Factor-β/Smad Signaling Pathway in Chronic Asthma Model

Targeted killing of myofibroblasts by biosurfactant di-rhamnolipid suggests a therapy against scar formation

Quantification of airway fibrosis in asthma by flow cytometry

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