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標題: LUC 抑制嗜中性白血球生成超氧自由基的研究
Inhibitory Effect of LUC on Superoxide Anion Generation in Neutrophils
作者: 莊文元
Chuang, Wen-Yuan
關鍵字: neutrophil;嗜中性白血球;superoxide;NADPH oxidase;超氧自由基
出版社: 生命科學系
本實驗評估新合成化合物 LUC 對於嗜中性白血球呼吸爆發作用的影響。LUC 以時間與濃度依存性方式抑制 formyl-Met-Leu-Phe (fMLP) 刺激大鼠嗜中性白血球產生超氧自由基,其 IC50 值為 4.5 ± 0.6 μM。LUC 抑制 fMLP 刺激嗜中性白血球產生超氧自由基的作用不具可逆性,並且對嗜中性白血球不產生細胞毒性。LUC 不會影響 phorbol 12-myristate 13-acetate (PMA) 刺激嗜中性白血球超氧自由基的生成。LUC 不會清除 dihy-droxyfurmaric acid (DHF) 自體氧化產生超氧自由基。LUC 不會影響 fMLP 刺激嗜中性白血球所產生的 p38 mitogen-activated protein kinase (MAPK)、extracellular signal-regulated kinase (ERK)、MAPK-activated protein kinase 2 (MAPKAPK2)、Akt(Thr308)、Akt(Ser473) 與 glycogen synthase kinase 3β(GSK3β) 的磷酸化作用。而LUC 會抑制蛋白質tyrosine磷酸化、phospholipase D (PLD) 的活性及細胞外 Ca2+ 流入,對這些訊息傳遞途徑的抑制作用可能參與了LUC阻斷 fMLP 刺激大鼠嗜中性白血球生成超氧自由基。

In the present study, the inhibition of superoxide anion generation by a novel synthetic compound LUC in rat neutrophils was examined. LUC inhibited formyl-Met-Leu-Phe (fMLP)-induced superoxide anion genera¬tion in a time- and concentration-dependent manner with an IC50 value of 4.5 ± 0.6 μM. LUC had no effect on phorbol 12-myristate 13-acetate (PMA)-induced response. Inhibition by LUC was irreversible and not caused by cytotoxic effect. LUC did not scavenge the generated superoxide during dihydroxyfumaric acid (DHF) autoxidation. LUC had no effect on the phosphorylation of p38 mito¬gen-activated protein kinase (MAPK)、extracellular signal-regulated kinase (ERK)、MAPK-activated protein kinase 2 (MAPKAPK2)、Akt(Thr308)、Akt(Ser473) and glycogen synthase kinase 3β(GSK3β) in response to fMLP stimulation. However, LUC attenu¬ated the fMLP-induced protein tyrosine phosphorylation and phospholipase D (PLD) activity, and blocked extracellu-lar Ca2+ entry. Inhibition of these signaling pathways is probably responsible for the inhibition of fMLP-induced superoxide anion generation by LUC in rat neutro¬phils.
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