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dc.contributorShu-Peng Hoen_US
dc.contributor.authorYen-Chun Pengen_US
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dc.description.abstract背景與目的:發炎相關的癌症是對於癌症防治的重要議題,幽門桿菌、胃炎與胃癌序列關係則是此類疾病最重要的疾病模式之一。近年來對於防治胃癌的共識為主要的策略就是根除幽門桿菌,本研究就臨床與分子觀點探討藥物與幽門桿菌對胃黏膜影響的微觀環境改變與分子效應。 研究方法:第一部分胃黏膜病理部份,收集病人有或無服用質子幫浦阻斷劑進行分析,以內視鏡切片術胃竇部黏膜組織,以福馬林保存送病理切片,再進一步進行病理染色。以雪梨胃炎分類系統為準則對胃黏膜的病理進行分析。第二部分藥物(omeprazole與clarithromycin)對於幽門桿菌在胃上皮細胞株的作用分析。以幽門桿菌萃取物處理細胞株,以兩株不同幽門桿菌株ATCC 43504 (cag A陽性) 與 ATCC 51932 (cag A陰性) 幽門桿菌菌體萃取物處理胃癌細胞株Kato-III,以西方墨點試驗觀察轉錄因子NF-κB活化有關之蛋白質的變化。以反轉錄聚合酶鏈式反應進行NF-κB相關細胞激素的表現。 結果: 第一部分共收集76位個案進行分析,其中44胃個案幽門桿菌感染,19位服用質子幫浦阻斷劑。服用質子幫浦阻斷劑組病人之胃黏膜中性球浸潤有較少白血球浸潤與淋巴球浸潤的現象,質子幫浦阻斷劑組有顯著的胃黏膜萎縮的現象,對於胃黏膜的腸道化生影響則無顯著的影響。以服用時間分析,病人服用質子幫浦阻斷劑時間愈長,胃黏膜中性球的浸潤愈少,此外,服用質子幫浦阻斷劑的時間對於胃黏膜幽門桿菌的數量有顯著的抑制作用。第二部分:幽門桿菌與omeprazole都會影響NF-κB與IkB的磷酸化的表現,幽門桿菌株ATCC 43504 (cag A陽性) 與 ATCC 51932 (cag A陰性)菌體萃取物處理胃癌細胞株Kato-III,NF-κB的表現會受到幽門桿菌的刺激而表現增加。也會誘發NF-κB相關細胞激素COX-2基因表現,但對於IL-6與IL-8不會誘發表現。Omeprazole只會抑制cagA陰性幽門桿菌所誘發的NF-κB表現。CagA陽性幽門桿菌所誘發的COX-2會被omeprazole所增強表現, CagA陰性幽門桿菌所誘發的COX-2會被omeprazole所抑制。若使用clarithromycin與幽門桿菌共同處理過的細胞,也發現的NF-κB 的表現降低。單獨使用clarithromycin處理, NF-κB 的基本表現量也會降低。細胞株經過48小時clarithromycin與幽門桿菌株 ATCC 43504 (cag A-positive)與ATCC 51932 (cag A-negative)的處理,降低 IL-8 mRNA 的表現。根據NF-κB傳統路徑有關的蛋白p65與替代路徑有關的蛋白p52,可被幽門桿菌活化,但被clarithromycin降解。 結論: 服用質子幫浦阻斷組病人之胃黏膜中性球浸潤有較少白血球浸潤與淋巴球浸潤,且有顯著的胃黏膜萎縮的現象。cag A陽性與cag A陰性幽門桿菌株皆可活化NF-κB的表現。Omeprazole對於幽門桿菌所處理為細胞株的NF-κB與相關細胞激素呈多型性影響。Clarithromycin則可透過傳統與替代路徑調控幽門桿菌所活化的NF-κB與IL-8zh_TW
dc.description.abstractBackground and aims:Inflammation associated cancer is one of the important issues in cacer prevention. Helicobacter pylori (H. pylori) related gastritis and cancer is one of the important disease models of inflammation assoicated cancer. The statement that eradication of H. pylori is the most effective method of primary prevention for gastric cancer. It the present study, we aimed to eludicate the interaction of drugs with H. pylori in the gastric microenviroment and molecular mechanism. Materials and Methods: The first part: Adult patients taking proton pump inhibitors (PPI)or not who received upper gastrointestinal endoscopy were enrolled. Endoscopic biopsies of gastric antral mucosa were performed and evaluated by H&E stain according to the update Sydney system. The second part: effect of omeprazole and clarithromycin on Kato-III cell line, which were stimulated with H. pylori water extracts (HPE) containing ATCC 43504(CagA+) and ATCC 51932(CagA-) strains. NF-κB activation, IκB expression and phosphorylation, and the cytokines expression were assessed in the absence and presence of omeprazole or clarithromycin. Results: The first part: Among the 76 patients, 44 patients had H. pylori infection and 19 patients had taken PPI prior to gastric biopsy with varying duration. Patients who taking PPI had significant less neutrophil and lymphomcyte infiltration in gastric mucosa, more gastric mucosa atrophy. Duration of PPI use is reversely correlated with neutrophil and H. pylori infiltration of gastric mucosa. The second part: Both H. pylori and ompeprazole affect NF-κB activation and IκB phosphorylation. CagA+and CagA- H. pylori induced NF-κB activation and COX-2 expression, whereas omeprazole suppressed NF-κB activation in the CagA- strain. CagA+ and CagA- HPE induced COX-2 expression, but no significant effect on IL-6 and IL-8. However, OMP downregulated the transcription of COX-2, IL-6, and IL-8 in CagA- HPE treated cells. Clarithromycin inhibited H. pylori-induced activation of NF-κB and associated upregulation of IL-8 expression. H. pylori activated NF-κB classical pathway associated protein p65 and alternative pathway protein p52, and clarithromycin degradated them. Cnclusion: PPI use is associated with less neutrophil and lymphocyte infltration of gastric mucosa, and related to the atrophy of mucosa. H. pylori induces NF-κB activation in a CagA-independent manner. CagA of H. pylori exerted different behavior of H. pylori induced NF-κB activation and associated cytokines expression. However, OMP suppressed NF-κB activation and associated cytokines also differently in CagA+ and CagA- HPE treated Kato-III cells. H. pylori-induced NF-κB signaling can occur through classical and alternative activation pathways, and CAM inhibits NF-κB these two pathways.en_US
dc.description.tableofcontents中文摘要 i 英文摘要 iii 目 次 v 表目次 vi 圖目次 vii 第一章 緒論 1 第一節 引言與背景簡介 1 第二節 研究假說 10 第三節 實驗研究設計 10 第二章 質子幫浦阻斷劑對胃黏膜微環境影響 16 第一節 前言 16 第二節 材料與方法 17 第三節 結果 18 第四節 討論 19 第三章Omeprazole與幽門桿菌在胃黏膜的相互作用 28 第一章前言 28 第二節 材料與方法 30 第三節 結果 31 第四節 討論 32 第四章Clarithromycin幽門桿菌在胃黏膜的相互作用 40 第一節 前言 40 第二節 材料與方法 42 第三節 結果 44 第四節 討論 45 第五章、結論 56 第一節 研究主要發現 56 第二節 研究特色與貢獻 57 第三節 未來展望 59 參考書目 61zh_TW
dc.subjectHelicobacter pylorien_US
dc.subjectproton pump inhibitoren_US
dc.titleInteraction of Omeprazole and Clarithromycin with Helicobacter pylori in Gastric Mucosa Microenviromenten_US
dc.typeThesis and Dissertationen_US
item.openairetypeThesis and Dissertation-
item.fulltextwith fulltext-
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