کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2052517 | 1074233 | 2005 | 7 صفحه PDF | دانلود رایگان |
We hypothesized that catecholamines through β-adrenoceptor might modulate macrophage function. We showed that isoproterenol concentration-dependently induced HO-1 production through β1-but not β2-adrenoceptor. Production was increased by forskolin and inhibited by pretreatment with the PKA inhibitor, H-89. Furthermore, induction of HO-1 by isoproterenol effectively protected RAW264.7 cells from effects of glucose oxidase treatment, which was abrogated either by HO-1 inhibitor, ZnPP IX and β-adenoceptor antagonist, propranolol. Thus, stimulation of HO-1 production through β1-adenoceptors, and via the PKA pathways by isoproterenol, can enable RAW264.7 cells to resist oxidant stress, suggesting that catecholamine hormones may be necessary, at least, to maximize defending role of macrophages.
Journal: FEBS Letters - Volume 579, Issue 25, 24 October 2005, Pages 5494–5500