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Ok Hee Chai

Bio: Ok Hee Chai is an academic researcher from Chonbuk National University. The author has contributed to research in topics: Histamine & Mast cell. The author has an hindex of 18, co-authored 67 publications receiving 1001 citations.


Papers
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Journal ArticleDOI
TL;DR: A protective role of PPARγ is demonstrated in the pathogenesis of the asthma phenotype through regulation of PTEN expression throughregulation of phosphatase and tensin homologue deleted on chromosome ten.
Abstract: The ligand-activated nuclear receptor peroxisome proliferator-activated receptor gamma (PPARgamma) has been shown to regulate cell activation, differentiation, proliferation, and/or apoptosis. PPARgamma is also associated with anti-inflammatory responses. However, the signaling mechanism remains elusive. We have used a mouse model for asthma to determine the effect of PPARgamma agonists, rosiglitazone or pioglitazone, and PPARgamma on allergen-induced bronchial inflammation and airway hyperresponsiveness. Administration of PPARgamma agonists or adenovirus carrying PPARgamma cDNA (AdPPARgamma) reduced bronchial inflammation and airway hyperresponsiveness. Expression of PPARgamma was increased by ovalbumin (OVA) inhalation, and the increase was further enhanced by the administration of the PPARgamma agonists or AdPPARgamma. Levels of IL-4, IL-5, IL-13, and eosinophil cationic protein were increased after OVA inhalation, and the increased levels were significantly reduced by the administration of PPARgamma agonists or AdPPARgamma. The results also showed that the administration of PPARgamma agonists or AdPPARgamma up-regulated phosphatase and tensin homologue deleted on chromosome ten (PTEN) expression in allergen-induced asthmatic lungs. This up-regulation correlated with decreased phosphatidylinositol 3-kinase activity as measured by reduced phosphorylation of Akt. These findings demonstrate a protective role of PPARgamma in the pathogenesis of the asthma phenotype through regulation of PTEN expression.

131 citations

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TL;DR: Results suggest that Houttuynia cordata THUNB water extract may be beneficial in the treatment of mast cell-mediated anaphylactic responses.
Abstract: The present study was investigated the effect of Houttuynia cordata THUNB water extract (HCWE) on mast cell-mediated anaphylactic reactions. The mast cell-mediated anaphylactic reaction is involved in many allergic diseases such as asthma and allergic rhinitis. HCWE has been used as a traditional medicine in Korea and is known to have an antioxidant and anti-cancer activities. However, its specific effect of mast cell-mediated anaphylactic reactions is still unknown. We examined whether HCWE could inhibit compound 48/80-induced systemic anaphylaxis, IgE-mediated passive cutaneous anaphylaxis (PCA), and mast cell activation. The oral administration of HCWE inhibited compound 48/80-induced systemic anaphylaxis in mice. HCWE also inhibited the local allergic reaction, PCA, activated by anti-dinitrophenyl (DNP) IgE antibody in rats. HCWE reduced the compound 48/80-induced mast cell degranulation and colchicine-induced deformation of rat peritoneal mast cells (RPMC). Moreover, HCWE dose-dependently inhibited histamine release and calcium uptake of RPMC induced by compound 48/80 or anti-DNP IgE. HCWE increased the level of intracellular cAMP and inhibited significantly the compound 48/80-induced cAMP reduction in RPMC. These results suggest that HCWE may be beneficial in the treatment of mast cell-mediated anaphylactic responses.

101 citations

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TL;DR: These results suggest that mast cells modulate vascular permeability by the regulation of the PI3K-HIF-1alpha-VEGF axis.
Abstract: Rationale: Bronchial inflammation is usually accompanied by increased vascular permeability. Mast cells release a number of mediators that act directly on the vasculature, resulting in vasodilatation, increased permeability, and subsequent plasma protein extravasation. Vascular endothelial growth factor (VEGF) has been implicated to contribute to asthmatic tissue edema through its effect on vascular permeability. However, the effects of mast cells on VEGF-mediated signaling in allergic airway disease are not clearly understood.Objectives: An aim of the present study was to investigate the role of mast cells on VEGF-mediated signal transduction in allergic airway disease.Methods: We used genetically mast cell–deficient WBB6F1-KitW/KitW-v (W/Wv) mice and the congenic normal WBB6F1+/+ mouse model for allergic airway disease to investigate the role of mast cells on VEGF-mediated signal transduction in allergic airway disease, more specifically in vascular permeability.Measurements and Main Results: Our presen...

57 citations

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TL;DR: Results corroborate the finding that curcumin may have anti-allergic activity and significantly attenuated the mast cell-mediated passive cutaneous anaphylactoid reaction in an animal model.
Abstract: Mast cells participate in allergies and inflammation by secreting a variety of pro-inflammatory mediators. Curcumin, the active component of turmeric, is a polyphenolic phytochemical with anti-tumor, anti-inflammatory, anti-oxidative, and anti-allergic properties. The effects of curcumin on compound 48/80-induced mast cell activation and passive cutaneous anaphylactoid reactions are unknown. In this report, we investigated the influences of curcumin on the passive cutaneous anaphylactoid response in vivo and compound 48/80-induced mast cell activation in vitro. The mechanism of action was examined by calcium uptake measurements and cAMP assays in mast cells. Curcumin significantly attenuated the mast cell-mediated passive cutaneous anaphylactoid reaction in an animal model. In agreement with this in vivo activity, curcumin suppressed compound 48/80-induced rat peritoneal mast cell (RPMC) degranulation and histamine release from RPMCs. Moreover, compound 48/80-elicited calcium uptake into RPMCs was reduced in a dose-dependent manner by curcumin. Furthermore, curcumin increased the level of intracellular cAMP and significantly inhibited the compound 48/80-induced reduction of cAMP in RPMCs. These results corroborate the finding that curcumin may have anti-allergic activity.

56 citations

Journal ArticleDOI
TL;DR: The effect of GA on airway inflammation and expression of Th1, Th2 and Th17 cytokines in an ovalbumin (OVA)‐induced AR mouse model suggest that GA may be used as a therapeutic agent for AR.

47 citations


Cited by
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Journal Article
TL;DR: The book will undoubtedly be considered a classical contribution to medical literature and is strongly recommended, not only because of the general interest of its topic, but as a reference book on penicillin therapy of hitherto unequalled excellence.
Abstract: MEDICAL LITERATURE has been deluged during the past few years with books and papers on penicillin; but a book which has been produced under the general editorship of Sir Alexander Fleming himself represents a complete and authoritative summary of penicillin therapy as it stands today.' The book contains a series of independent contributions by \"experienced and eminent men who have worked with penicillin in Great Britain\". Their opinions and practical methods differ slightly, and there is some overlapping; but these are not disadvantageous, comparison and contrast lending interest to the reading. In the first or general section of the book Fleming contributes two chapters, one on the history and development of penicillin, introducing some interesting sidelights in the romance of discovery, the other on the bacteriological control of penicillin therapy. In both chapters the information is set out in meticulous detail and with a clarity and simplicity which can be enjoyed by all readers. Fleming also gives the right perspective to the place of penicillin amongst the antibiotics and lays down the principles of treatment. Both chapters are well illustrated and are the most outstanding in the book. Included in this first section also are chapters on the chemistry and manufacture of penicillin and its pharmacy, pharmacology and methods of administration. The second section of the book is entirely clinical, giving each author's view on the use of penicillin therapy in a disease or an infection of some particular region of the body. The entire range of peniCillin-sensitive conditions is considered in twenty authoritative and clearly written chapters; these contain many references and illustrations. Dental and veterinary diseases are also given fairly full consideration. The final section is a condensed resume of much of the preceding chapters and is written for. the general practttioner. This chapter is superttuous: it does not contain enough detall to be of much practical value. The book as a Whole, however, will undoubtedly be considered a classical contribution to medical literature and is strongly recommended, not only because of the general interest of its topic, but as a reference book on penicillin therapy of hitherto unequalled excellence. The typography, although conforming to war economy standards, is clear and the paper is good. There is an excellent list of references and the index is satisfactory.

1,657 citations

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TL;DR: A translational overview on the biological basis of atrial remodeling and the proarrhythmic mechanisms involved in the fibrillation process is given.
Abstract: Atrial fibrillation (AF) is an arrhythmia that can occur as the result of numerous different pathophysiological processes in the atria. Some aspects of the morphological and electrophysiological al...

1,051 citations

Journal Article

953 citations

Journal ArticleDOI
TL;DR: The molecular mechanisms through which PPARs regulate transcription are thoroughly addressed with particular emphasis on the latest results on corepressor and coactivator action and how the integration of various intra-cellular signaling pathways allowsPPARs to participate to whole-body homeostasis by mediating regulatory crosstalks between organs.

721 citations

Journal ArticleDOI
TL;DR: It has become clear that HIF promotes the bactericidal activities of phagocytic cells and supports the innate immune functions of dendritic cells, mast cells and epithelial cells, highlighting an interdependence of the innateimmune and hypoxic responses to infection and tissue damage.
Abstract: At low levels of oxygen at sites of tissue infection, innate immune cells can adapt to survive and even enhance their antimicrobial functions. Recent studies show how this is controlled by hypoxia-inducible factor (HIF) downstream of nuclear factor-κB activation. Hypoxia-inducible factor (HIF) is an important transcriptional regulator of cell metabolism and the adaptation to cellular stress caused by oxygen deficiency (hypoxia). Phagocytic cells have an essential role in innate immune defence against pathogens and this is a battle that takes place mainly in the hypoxic microenvironments of infected tissues. It has now become clear that HIF promotes the bactericidal activities of phagocytic cells and supports the innate immune functions of dendritic cells, mast cells and epithelial cells. In response to microbial pathogens, HIF expression is upregulated through pathways involving the key immune response regulator nuclear factor-κB, highlighting an interdependence of the innate immune and hypoxic responses to infection and tissue damage. In turn, HIF-driven innate immune responses have important consequences for both the pathogen and the host, such that the tissue microenvironment fundamentally influences susceptibility to infectious disease.

653 citations