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    請使用永久網址來引用或連結此文件: http://libir.tmu.edu.tw/handle/987654321/6542


    題名: 麩醯胺或精胺酸添加對發炎反應引發免疫黏著分子表現及白血球遷移之影響
    Effects of glutamine or arginine on inflammatory-induced adhesion molecule expression and leukocyte migration
    作者: 葉秋莉
    Chiu Li Yeh
    貢獻者: 藥學研究所
    關鍵詞: 敗血症
    麩醯胺
    精胺酸
    白血球
    黏著分子
    淋巴球
    sepsis
    glutamine
    arginine
    adhesion molecule
    polymorphonuclear neutrophils transmigration
    interleukin-8
    nitric oxide
    日期: 2005
    上傳時間: 2009-09-11 16:58:52 (UTC+8)
    摘要: 本研究分成動物實驗及細胞培養兩部分，動物實驗主要觀察以glutamine (GLN)或arginine (Arg)介入對敗血症黏著分子及發炎反應相關介質的影響。細胞培養實驗將人類臍帶靜脈內皮細胞(human umbilical vein endothelial cells, HUVECs)及中性多形核白血球(polymorphonuclear neutrophils, PMNs)培養於不同濃度的GLN或Arg中，以腹部手術病人的血漿及腹腔沖洗液(peritoneal drain fluid, PDF)刺激後，觀察細胞上黏著分子、細胞激素及接受器的表現，並觀察PMNs穿過HUVEC轉移的情形。在GLN介入的動物實驗結果顯示，與控制組比較，GLN組降低循環血中的intercellular adhesion molecule (ICAM)-1濃度，器官中myeoloperoxidase (MPO)的活性及肝外器官中interleukin (IL)-6的表現，淋巴球內interferon (IFN)-γ濃度較高而IL-4則較低，此結果顯示GLN使敗血症時發炎反應趨緩，體內Th1/Th2平衡趨向Th1。細胞培養實驗結果顯示HUVEC及PMNs上的免疫黏著分子及整合素會被腹部手術病人的血漿及PDF刺激而表現。與低濃度(300uM)相較，GLN在接近人類正常生理濃度(600μM)及高於生理濃度(1000μM)時，會降低因病人體液刺激所表現的免疫黏著分子、整合素、IL-8濃度及PMNs轉移的數目。在Arg介入的動物實驗結果顯示，與控制組比較，Arg組增加循環血中的ICAM-1濃度，器官中
    MPO的活性及肝外器官中IL-6的表現，淋巴球內IFN-γ濃度較低而IL-4則較高，此結果顯示Arg使敗血症時發炎反應增加，體內Th1/Th2平衡較趨向於Th2。細胞培養實驗結果顯示與低濃度(50uM)相較，Arg在接近人類正常生理濃度(100μM)時，會降低因病人體液刺激所表現的免疫黏著分子、整合素、IL-8濃度及PMNs轉移的數目，在高於生理濃度(1000μM)時降低的情況更為明顯。在給予NO synthase抑制劑(LNMMA)後，則100uM及1000 uM在黏著分子表現及PMNs遷移的結果均與50 uM相同。此結果顯示NO在HUVEC及PMNs受到刺激時對黏著分子表現及PMNs發生轉移的作用扮演非常重要的調節角色。
    There were two parts in this study. The animal studies investigated the effects of glutamine (GLN) or arginine (Arg) on plasma intracellular adhesion molecule (ICAM)-1 levels and leukocyte integrin expressions in gut-derived sepsis. Myeloperoxidase (MPO) activities in organs were also analyzed to identify the extent of tissue injury resulting from neutrophil infiltration. The in vitro studies investigated the effect of different GLN or Arg concentrations on surface molecule expression on endothelial cells (ECs) and leukocytes and the transendothelial migration of polymorphonuclear neutrophils (PMNs) through ECs stimulated by plasma or peritoneal drain fluid (PDF) from a surgical patient. The results of GLN intervention in septic mice showed that, GLN administration may enhance lymphocyte function, reduced interleukin (IL)-6 levels in organs, attenuate the PMN-endothelium interactions and may consequently decrease neutrophil infiltration into tissues. The GLN in vitro study suggests that ECs and PMNs were activated after patient’s plasma or PDF stimulation. A low GLN concentration comparable to catabolic conditions (300 uM) resulted in higher adhesion molecule expression and greater transendothelial migration of neutrophils. GLN administration at levels similar to (600 uM) or higher than physiologic concentrations (1000 uM) reduced IL-8 and adhesion molecule expression, and PMN transmigration was also decreased after stimulation with plasma or PDF from a surgical patient. The results of Arg intervention in septic mice showed that, Arg administration increased CAM expression, enhanced MPO activities in organs and aggravated the PMN-endothelium interactions in septic condition. The Arg in vitro study suggests that a low Arg concentration comparable to catabolic conditions (50 uM) resulted in higher adhesion molecule expression and greater transendothelial migration of neutrophils. Arg administration at levels similar to physiologic concentrations (100 uM) reduced IL-8 and adhesion molecule expression, and PMN transmigration was also decreased. High Arg concentration (1000 uM) had greater reduction effect on CAM expression and PMNs migration after stimulation with body fluid from a surgical patient. There were no differences in CAM and IL-8 expressions in groups incubated with different Arg concentration when nitric oxide (NO) synthase inhibitor (LNMMA) was added in the medium. This result suggests that NO plays an important role in modulating CAM expression and PMNs transmigration.
    資料類型: thesis
    顯示於類別:[藥學系] 博碩士論文

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