陳炳宏副教授(Bing-Hung Chen) - 高雄醫學大學生物科技學系

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研究肥大細胞去顆粒作用的分子調控機制:. 肥大細胞受到過敏原與IgE的刺激後,會將細胞質內的分泌型顆粒(secretory granules, SGs)經由胞吐 ... 繁體中文 English   搜尋... Menu 首頁Home 系學務訊息即時學系訊息.演講通知.作業考訊.工讀招募...等訊息通知(臉書) 活動剪影即時學系訊息.演講通知.作業考訊.工讀招募...等訊息通知(臉書) 系學生會即時學系訊息.演講通知.作業考訊.工讀招募...等訊息通知(臉書) 共用儀器預約 斑馬魚核心實驗室 登入 [僅限有發佈公告權限之註冊作者] 帳號 密碼 記得我 登入 首頁學系成員陳炳宏副教授(Bing-HungChen) 陳炳宏副教授(Bing-HungChen)   聯絡方式 辦公室:第一教學大樓N1023室 實驗室:第一教學大樓N1020室 電話:(07)3121101ext.2676 傳真:(07)3125339 電子郵件: [email protected] 其他個人網頁: 實驗室部落格(暫停維護) 臉書  學經歷 中山醫學大學醫事技術學系學士(1990) 美國維吉尼亞聯邦州立大學臨床實驗科學研究所碩士(1995) 美國維吉尼亞聯邦州立大學微生物與免疫學研究所博士(2001) 美國維吉尼亞聯邦州立大學微生物與免疫學研究所博士後研究(2001-2002) 國立清華大學生命科學院博士後研究(2002-2003) 高雄醫學大學蛋白質體中心學術合作組組長(2004-2006) 高雄醫學大學生物科技學系系主任(2012/08-2015/07) 主負責授課科目 生物科技導論 生物科技實驗 微生物學 免疫學 書報討論 專題研究 研究興趣 過敏與非過敏性發炎反應的分子生物學與細胞學的調控機制 抗過敏與抗發炎藥物之篩選與開發 肥大細胞與巨噬細胞之訊息傳遞機制研究 細胞脫顆粒作用調控   MechanisticRegulationofAllergicInflammatoryResponsesinMastCells 由於工業化以及飲食西化的影響,第一型即發型過敏性疾病的罹患率有逐年增加的趨勢。

此類過敏反應的成因,主要是由過敏原(如:花粉、塵蟎、花生、甲殼類海鮮、寵物皮屑等)所誘發B淋巴球製造的免疫球蛋白E(IgE),結合與促進肥大細胞或嗜鹼性球活化所造成的免疫疾病。

研究發現,經由活化Th2淋巴細胞或是其他發炎細胞(如:巨噬細胞)所分泌的細胞激素亦能直接或間接地造成過敏反應症狀的惡化。

目前臨床上常用的治療過敏方法,包括給予病患症狀舒緩藥劑(如:抗組織胺)、類固醇、以及新開發的抗IgE單株抗體,然而這些療法都各有其侷限或不足之處。

因此,本實驗室之主要研究方向為了解肥大細胞的活化機制,期望可以探索與開發具有抑制過敏性發炎的新型製劑。

           實驗室研究方向 調控過敏與發炎性免疫反應的分子生物學與細胞學機制 抗過敏與抗發炎藥物之篩選與開發 白血球訊息傳遞機制研究 設計與開發具醫療潛力的融合蛋白質   MechanisticRegulationofAllergicInflammatoryResponsesinMastCells 由於工業化以及飲食西化的影響,第一型即發型過敏性疾病的罹患率有逐年增加的趨勢。

此類過敏反應的成因,主要是由過敏原(如:花粉、塵蟎、花生、甲殼類海鮮、寵物皮屑等)所誘發B淋巴球製造的免疫球蛋白E(IgE),結合與促進肥大細胞或嗜鹼性球活化所造成的免疫疾病。

研究發現,經由活化Th2淋巴細胞或是其他發炎細胞(如:巨噬細胞)所分泌的細胞激素亦能直接或間接地造成過敏反應症狀的惡化。

目前臨床上常用的治療過敏方法,包括給予病患症狀舒緩藥劑(如:抗組織胺)、類固醇、以及新開發的抗IgE單株抗體,然而這些療法都各有其侷限或不足之處。

因此,本實驗室之主要研究方向為了解肥大細胞的活化機制,期望可以探索與開發具有抑制過敏性發炎的新型製劑。

    篩選新的抗過敏成份: 近年來,從天然食用與藥用植物中開發新的抗過敏成分已經逐漸受到重視。

我們利用囓齒類RBL-2H3與人類KU812肥大細胞株為篩選平台,分析不同的植物萃取物是否可以抑制這些細胞株因過敏原/IgE刺激所造成的活化現象(如:去顆粒化作用、胞內鈣離子變化、細胞激素基因表現等),以用來當做評估其抗過敏潛力的指標。

研究肥大細胞去顆粒作用的分子調控機制: 肥大細胞受到過敏原與IgE的刺激後,會將細胞質內的分泌型顆粒(secretorygranules,SGs)經由胞吐作用(exocytosis),將其中的各類型致敏性媒介物(例如:TNFalpha,MCP-1,IL-4)排放到胞外,因而導致過敏症狀的發生。

肥大細胞的胞吐作用又稱為去顆粒作用(degranulation)。

目前研究顯示,影響去顆粒作用的關鍵因子,包括了胞內鈣離子濃度以及分泌型顆粒能否與細胞膜進行融合。

此融合過程中,需要SGs與細胞膜上的不同蛋白質分子共同組成SNARE複合體(如:VAMP,SNAP,syntaxin);此外,SGs上的鈣離子偵測蛋白(如:synaptotagmin)在促進融合的過程也扮演著重要的調控角色。

目前,我們有興趣研究人類與小鼠的肥大細胞株在去顆粒過程中,SNARE複合物的形成與調控上的差異、參與肥大細胞去顆粒作用的SNARE複合物形成之分子調控機制。

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TheinterplayofCD23andADAM10anditsroleinIgEsynthesis.MathewsJ,ChenBH,ConradDH.The96thAnnualMeetingofTheAmericanAssociationofImmunologists,Seattle,Washington,2009.     專利 COMPOSITIONSANDMETHODSOFANTIALLERGICPHORBOLESTERANDPHORBOLDERIVATIVESASTHEMAINACTIVEINGREDIENTSFROMTHESEEDSOFAQUILARIAMALACCENSIS.(發明者:Fang-rongChang,Bing-hungChen,Hsue-yinHsu,ChenHsieh,Hui-pingHsieh;發佈日期:2017/9/21;專利局:US;專利編號:20170266250) 文章瀏覽點擊數 818308 主選單 Menu 學系簡介 學系成員 學生專區 畢業生流向調查 師生榮譽 實習就業 科學工業園區人才培育補助計畫 招生訊息 新生專區 表單下載 聯絡我們 常用連結 Menu KMU首頁 KMU生命科學院 KMU臉書(官方版) KMU圖書資訊處 KMU電子資源查詢系統 KMU校務資訊系統 KMU公文整合系統 KMU數位學習系統 KMU課程互動系統(IRS) KMUWebGuide 教育部 科技部 2019© 高雄醫學大學生命科學院生物科技學系建議使用Chrome/Safari/Firefox瀏覽 地址:高雄市80708三民區十全一路100號高雄醫學大學生物科技學系 位置:第一教學大樓9,10樓(系辦公室:N943) 電話:07-3121101分機2709 傳真:07-3125339 信箱:[email protected]   Gototop



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