中國醫藥大學機構典藏 China Medical University Repository, Taiwan:Item 310903500/28718
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    题名: Evaluation of four prescriptions of Traditional Chinese Medicine: Syh-Mo-Yiin, Guizhi-Fuling-Wan, Shieh-Qing-Wan and Syh-Nih-Sann on experimental acute liver damage in rats
    作者: Tsai, CC;Kao, CT;Hsu, CT;Lin, CC;Lin, JG
    贡献者: 中醫學院中醫所;CHINA MED COLL,RES INST CHINESE MED,TAICHUNG,TAIWAN;CHINA MED COLL,DEPT PATHOL,TAICHUNG,TAIWAN;KAOHSIUNG MED COLL,GRAD INST NAT PROD,KAOHSIUNG,TAIWAN
    日期: 1997
    上传时间: 2010-09-24 13:43:55 (UTC+8)
    出版者: ELSEVIER SCI IRELAND LTD
    摘要: 1 The possible mechanisms of action of the inhibitory effect of abruquinone A on the respiratory burst in rat neutrophils in vitro was investigated. 2 Abruquinone A caused an irreversible and a concentration-dependent inhibition of formylmethionyl-leucyl-phenylalanine (fMLP) plus dihydrocytochalasin B (CB)- and phorbol 12-myristate 13-acetate (PMA)-induced superoxide anion (O-2(.-)) generation with IC50 values of 0.33+/-0.05 mu g ml(-1) and 0.49+/-0.04 mu g ml(-1), respectively. 3 Abruquinone A also inhibited O-2 consumption in neutrophils in response to fMLP/CB and PMA. However, abruquinone A did not scavenge the generated O-2(.-) in xanthine-xanthine oxidase system and during dihydroxyfumaric acid (DHF) autoxidation. 4 Abruquinone A inhibited both the transient elevation of [Ca2+](i) in the absence of [Ca2+](o) (IC50 7.8+/-0.2 mu g ml(-1)) and the generation of inositol trisphosphate (IP3) (IC50 10.6+/-2.0 mu g ml(-1)) in response to fMLP. 5 Abruquinone A did not affect the enzyme activities of neutrophil cytosolic protein kinase C (PKC) and porcine heart protein kinase A (PKA). 6 Abruquinone A had no effect on intracellular guanosine 3':5'-cyclic monophosphate (cyclic GMP) levels but decreased the adenosine 3':5'-cyclic monophosphate (cyclic AMP) levels. 7 The cellular formation of phosphatidic acid (PA) and phosphatidylethanol (PEt) induced by fMLP/CB was inhibited by abruquinone A with IC50 values of 2.2+/-0.6 mu g ml(-1) and 2.5+/-0.3 mu g ml(-1), respectively. Abruquinone A did not inhibit the fMLP/CB-induced protein tyrosine phosphorylation but induced additional phosphotyrosine accumulation on proteins of 73-78 kDa in activated neutrophils. 8 Abruquinone A inhibited both the O-2(.-) generation in PMA-activated neutrophil particulate NADPH oxidase (IC50 0.6+/-0.1 mu g ml(-1)) and the iodonitrotetrazolium violet (INT) reduction in arachidonic acid (AA)-activated cell-free system (IC50 1.5+/-0.2 mu g ml(-1)). 9 Collectively, these results indicate that the inhibition of respiratory burst in rat neutrophils by abruquinone A is mediated partly by the blockade of phospholipase C (PLC) and phospholipase D (PLD) pathways, and by suppressing the function of NADPH oxidase through the interruption of electron transport.
    關聯: JOURNAL OF ETHNOPHARMACOLOGY 55(3):213-222
    显示于类别:[中國醫學研究所] 期刊論文

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