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KMID : 0043319950180040262
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Archives of Pharmacal Research
1995 Volume.18 No. 4 p.262 ~ p.266
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The Involvement of Protein Tyrosine Kinase in the Bacterial Lipopolysaccharide-Induced Arachidonic Acid Metabolism in Rat Alveolar Macrophages
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Kim Ji-Young
Lee Soo-Hwan
Lee Ji-Young
Moon Chang-Hyun
Lim Jong-Seok
Moon Chang-Kiu
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Abstract
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Bacterial lipopolysaccharide (LPS) is one of the most potent inducers of various cytokines nad other proinflammatory mediators in macrophages. Although pathophysiological consequences of LPS-induced responses are well established, the mechanisms through which LPS-generated singals are transduced remain unclear. In the present study, we attempted to determine early intracellular events after LPS binding which transduced the signal for the induction of arachidonic acid metabolism in rat alveolar macrophages. While H-7, a protein kinase C(PKC) inhibitor, did not affect LPS-stimulated prostaglandin synthesis, staurosporine enhanced archidonic acid etabolism in macropahages treated with LPS. Phorbol-12-myristate-13 acetate snesitive to LPS compare with control group. PMA and H-7 did not alter the effect of flucose. Pertussis toxin did not show nay effect, thus pertussis toxin snesitive G-protein pathway appears not to play a role in this experimental system. Genistein and tyrphostin 25, protein tyrosine kinase 9PTK) inhibitors, markedly inhibited prostaglandin synthesis in macrophages nal transduction events leading to icnreased macrophage arachidonic acid metabolism.
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KEYWORD
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Lipopolysacchride, Arachidonic acid metabolism, Alveolar macrophage, Protein Kinase C, Protein tyrosine kinase
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