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    Please use this identifier to cite or link to this item: https://ir.fy.edu.tw:8080/ir/handle/987654321/9510


    Title: 2-hydroxymethyl-1-naphthol diacetate (TAC) suppresses the superoxide anion generation in rat neutrophils.
    Authors: Jih-Pyang Wang, Lo-Ti Tsao, Ai-Yu Shen, Shu-Ling Raung.
    Contributors: 輔英科技大學 物理治療系
    Keywords: TAC;Neutrophil;Respiratory burst;NADPH oxidase;Protein kinase C;Phospholipase D;Mitogen-activated protein kinase;Translocation;Phospholipase C;Inositol phosphate;Intracellular Ca2+ concentration
    Date: 1999-03-01
    Issue Date: 2010-11-10 09:42:39 (UTC+8)
    Abstract: We have investigated the inhibitory effect of 2-hydroxymethyl-1-naphthol diacetate (TAC) on the respiratory burst of rat neutrophils and the underlying mechanism of action was also assessed in this study. TAC caused concentration-related inhibition of the formylmethionyl-leucyl-phenylalanine (fMLP) plus dihydrocytochalasin B (CB)- and phorbol 12-myristate 13-acetate (PMA)-induced superoxide anion (O2•−) generation (IC50 10.2 ± 2.3 and 14.1 ± 2.4 μM, respectively) and O2 consumption (IC50 9.6 ± 2.9 and 13.3 ± 2.7 μM, respectively) of neutrophils. TAC did not scavenge the generated O2•− during dihydroxyfumaric acid autoxidation. TAC inhibited both the transient elevation of [Ca2+]i in the presence or absence of [Ca2+]o (IC50 75.9 ± 8.9 and 84.7 ± 7.9 μM, respectively) and the generation of inositol trisphosphate (IP3) (IC50 72.0 ± 9.7 μM) in response to fMLP. Cytosolic phospholipase C (PLC) activity was also reduced by TAC at a same range of concentrations. The PMA-induced PKC-β associated to membrane was attenuated by TAC (about 80% inhibition at 30 μM). Upon exposure to fMLP, the cellular cyclic AMP level was decreased in neutrophils pretreated with TAC. TAC attenuated fMLP-induced phosphorylation of mitogen-activated protein kinase (MAPK) p42/44 (IC50 17.4 ± 1.7 μM), but not p38. The cellular formation of phosphatidic acid (PA) and, in the presence of ethanol, phosphatidylethanol (PEt) induced by fMLP was inhibited by TAC in a concentration-dependent manner (IC50 25.4 ± 2.4 and 25.9 ± 1.4 μM, respectively). TAC had no effect on the O2•− generation of PMA-stimulated and arachidonic acid (AA)-stimulated NADPH oxidase preparations. However, TAC caused concentration-related decrease of the membrane associated p47phox in PMA-stimulated neutrophils (about 80% inhibition at 30 μM). We conclude that inhibition by TAC of the neutrophil respiratory burst is probably attributable to the blockade of the p42/44 MAPK and phospholipase D (PLD) pathways, the membrane translocation of PKC, and to the failure in assembly of a functional NADPH oxidase complex. Blockade of the PLC pathway by TAC probably plays a minor role.
    Relation: Free Radic. Biol. Med. 26(7-8),1010-1018
    Appears in Collections:[物理治療系] 期刊論文

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