• Title/Summary/Keyword: Eosinophil apoptosis

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The effects of Gamisipjeontang-gamibang on injured tissue after burn elicitation (가미십전탕(加味十全湯) 가미방(加味方)이 화상(火傷)의 조직 손상에 미치는 영향)

  • Kim, Hee-Young;Hong, Seung-Ug
    • The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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    • v.22 no.1
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    • pp.62-75
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    • 2009
  • Objective : The purpose of this study is to examine the effects of Gamisipjeontang-gamibang(GT) on an experimental bum elicitation. Method : The absorbance of the photo cell mixed with GT at the Abs 560 nm was measured after irradiation for 1 min. In order to know the antioxidant effect on skin cell of mice after burn elicitation, superoxide dismutase(SOD) activity was measured. Also, in order to know effects on the skin regeneration in the burned mice, we counted the eosinophil in blood from animals via cardiac puncture and observed the histological structure in the epidermal basal layer and the dermal section on the 3rd, 7th and 14th day after burn elicitation. We also studied changes in angiogenesis in the capillary surrounding the basal layer and dermal papilla. The changes of HSP70 distribution and changes of p53 positive reaction were observed to investigate the changes of the stress in the skin as well. Result : The results indicated that GT has a significant impact on the antioxidant effect on skin cells of mice after bum elicitation by increasing SOD activity in vitro test. GT seems to decrease MIP-2 which induces neutrophil infiltration and promotes the angiogenesis dose-dependently. Furthermore, GT decreased HSP70, the expression of which was induced by elevated temperatures, and p53 which induce a apoptosis after stress. Conclusion : GT can be applied to burned skin through its antioxidant effect and skin regeneration property.

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Novel glutathione-containing dry-yeast extracts inhibit eosinophilia and mucus overproduction in a murine model of asthma

  • Kim, Yun-Ho;Choi1, Yean-Jung;Lee, Eun-Jung;Kang, Min-Kyung;Park, Sin-Hye;Kim, Dong Yeon;Oh, Hyeongjoo;Park, Sang-Jae;Kang, Young-Hee
    • Nutrition Research and Practice
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    • v.11 no.6
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    • pp.461-469
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    • 2017
  • BACKGROUND/OBSECTIVE: Airway inflammation by eosinophils, neutrophils and alveolar macrophages is a characteristic feature of asthma that leads to pathological subepithelial thickening and remodeling. Our previous study showed that oxidative stress in airways resulted in eosinophilia and epithelial apoptosis. The current study investigated whether glutathione-containing dry yeast extract (dry-YE) ameliorated eosinophilia, goblet cell hyperplasia and mucus overproduction. MATERIALS/METHOD: This study employed $2{\mu}g$/mL lipopolysaccharide (LPS)- or 20 ng/mL eotaxin-1-exposed human bronchial epithelial cells and ovalbumin (OVA)-challenged mice. Dry-YE employed in this study contained a significant amount of glutathione (140 mg in 100 g dry yeast). RESULTS: Human bronchial epithelial cell eotaxin-1 and mucin 5AC (MUC5AC) were markedly induced by the endotoxin LPS, which was dose-dependently attenuated by nontoxic dry-YE at 10-50 ${\mu}g$/mL. Moreover, dry-YE inhibited the MUC5AC induction enhanced by eotaxin-1, indicating that eotaxin-1-mediated eosinophilia may prompt the MUC5AC induction. Oral supplementation with 10-100 mg/kg dry-YE inhibited inflammatory cell accumulation in airway subepithelial regions with a reduction of lung tissue level of intracellular adhesion molecule-1. In addition, ${\geq}50$ mg/kg dry-YE diminished the lung tissue levels of eotaxin-1, eosinophil major basic protein and MUC5AC in OVA-exposed mice. Alcian blue/periodic acid schiff staining revealed that the dry-YE supplementation inhibited goblet cell hyperplasia and mucus overproduction in the trachea and bronchiolar airways of OVA-challenged mice. CONCLUSIONS: Oxidative stress may be involved in the induction of eotaxin-1 and MUC5AC by endotoxin episode and OVA challenge. Dry-YE effectively ameliorated oxidative stress-responsive epithelial eosinophilia and mucus-secreting goblet cell hyperplasia in cellular and murine models of asthma.