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研究生:蘇怡嘉
研究生(外文):Su, Yi-Chia
論文名稱:C18脂肪酸影響人類嗜中性白血球釋放超氧自由基和彈性蛋白酶的機轉探討
論文名稱(外文):Effects of C18 Fatty Acids on Superoxide Anion and Elastase Release in human Neutrophils
指導教授:黃聰龍黃聰龍引用關係
指導教授(外文):Hwang, Tsong-Long
學位類別:碩士
校院名稱:長庚大學
系所名稱:天然藥物研究所
學門:醫藥衛生學門
學類:藥學學類
論文種類:學術論文
論文出版年:2007
畢業學年度:95
語文別:中文
論文頁數:76
中文關鍵詞:嗜中性白血球C18脂肪酸超氧自由基彈性蛋白酶
外文關鍵詞:NeutrophilsElastase ReleaseC18 Fatty AcidsSuperoxide Anion
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摘要
從基礎到臨床,以及流行病學的調查,都觀察到FAs或FAs衍生物對細胞很重要。一般認為,維持FAs恆定的做法會是治療心血管疾病與發炎性疾病的有效方法。儘管如此,C18 FAs調節人類嗜中性白血球的生理功能仍未瞭解。本論文結果顯示,cis型態不飽合脂肪酸(USFAs)會抑制formyl-L-methionyl-L-leucyl-L-phenylalanine (FMLP)誘發人類嗜中性白血球釋放超氧自由基(O2•−)和彈性蛋白酶的作用以及加速鈣離子回復的現象,但是SFAs和trans結構的USFAs則不具有顯著影響。有趣地,隨著雙鍵數目增加,USFAs抑制效果逐漸減弱。cis型態甲基化的FAs則不具有抑制作用。另外,protein kinase (PK)C的活化劑在以thapsigargin活化人類嗜中性白血球時,會顯著抑制細胞內鈣離子和鋇離子濃度變化,而cis型態USFAs則不具有作用。這個結果顯示,PKC的抑制功能是經由抑制store-operated channel而來,cis型態USFAs的作用機轉則和PKC不同。有很多報告顯示,plasma membrane Ca2+-ATPase (PMCA)和Na+-Ca2+ exchanger (NCX)會降低活化態嗜中性白血球細胞內鈣離子濃度。將嗜中性白血球處理在無鈉的綬衝液中, cis 型態USFAs同樣具有抑制以FMLP活化嗜中性白血球產生的O2•−和加速鈣離子回復現象。值得注意,本論文在完整的嗜中性白血球或是萃取的細胞膜實驗模式中,cis型態USFAs都會顯著增加PMCA的活性;相反地,是SFAs、trans結構的USFAs以及甲基化的FAs都不具作用。綜合上述結果顯示,cis型態C18 USFAs抑制嗜中性白血球功能的作用機轉是經由活化細胞膜上PMCA的活性,進而降低細胞內鈣離子濃度而來。
Abstract
There is considerable evidence from clinical, experimental, and epidemiologic observations that fatty acids (FAs) play a critical role in cellular viability and manipulation of FA homeostasis may open novel therapeutic avenues to against cardiovascular disease and inflammatory syndromes. In spite of this, the physiological role of C18 FAs in regulating neutrophil functions remains poorly understood. In this thesis, cis C18 unsaturated (US)FAs, but not saturated (S)FAs and trans USFAs, were demonstrated to significantly inhibit the generation of superoxide anion (O2•−) and the release of elastase as well as to accelerate resequestration of cytosolic calcium in formyl-L-methionyl-L-leucyl-L-phenylalanine (FMLP)-activated human neutrophils. Interestingly, as increase in the number of double bound, the inhibitory actions of cis USFAs were weakened. Furthermore, cis USFAs with methyl ester did not share the inhibitions. In addition, the protein kinase (PK)C activator, but not cis USFAs, significantly altered cytosolic calcium and barium mobilization in thapsigargin-activated human neutrophils, suggesting that the inhibitory functions of PKC but not cis USFAs are through the inhibition of store-operated channel. A lot of reports have showed that plasma membrane Na+-Ca2+ exchanger and Ca2+-ATPase appear to be the primary contributors to clearance of cytosolic calcium in activated neutrophils. The role of Na+-Ca2+ exchanger was ruled out, since cis USFAs also inhibited the generation of O2•− and accelerated resequestration of cytosolic calcium in FMLP-activated human neutrophils in the sodium-free medium. Significantly, cis USFAs, but not saturated SFAs, trans USFAs, and USFAs with methyl ester, significantly increased the activities of plasma membrane Ca2+-ATPase in whole cells and isolated neutrophil membranes. In summary, the inhibition of human neutrophil functions by cis C18 USFAs in FMLP-activated human neutrophils are attributed to the blockade of calcium mobilization via the modulation of plasma membrane Ca2+-ATPase activities.
目錄
目錄…………………………………………………………………….1
縮寫表……………………………………………………………….....2
中文摘要.……………….…………………….......................................4
英文摘要……….………………………………………………............5
緒論………………………………………………………….……........6
實驗材料與方法……………………………………………………....13
結果……………………………………………………………………18
討論……………………………………………………………………24
圖表……………………………………………………………………27
參考文獻……………………………………………............................64
參考文獻
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5. 2-Benzoylamino-benzoicacid類似物影響人類嗜中性白血球釋出超氧自由基和彈性蛋白酶的機轉探討
6. FAL抑制嗜中性白血球生成超氧自由基的研究
7. 雙萜類衍生物與C18脂肪酸影響人類嗜中性白血球釋放超氧自由基和彈性蛋白酶的機轉探討
8. H2O7D與Ass-13-2a影響人類嗜中性白血球釋放超氧自由基和彈性蛋白酶酵素的機轉探討
9. 探討GMC抑制人類嗜中性白血球功能的藥理作用
10. EMR2影響人類嗜中性白血球訊息傳遞的機轉探討
11. 濱當歸活性成分imperatorin經由cAMP抑制人類嗜中性白血球釋放超氧自由基的探討
12. 玉蘭花、檄樹及咖啡等植物對基質金屬蛋白酶及彈性蛋白酶作用之探討
13. 探討菲律賓胡椒萃取物PP-6與化合物HCL-85抑制人類嗜中性白血球釋出超氧自由基之機轉
14. 胰臟彈性蛋白酶的特性及功能性研究與其臨床應用
15. 探討在嗜中性白血球CYL-26z抑制phospholipaseD活化,artocarpolA促進生成超氧自由基及formylpeptide活化phosphoinositide3-kinase的作用機制