Abstract
We hypothesized that catecholamines through β-adrenoceptor might modulate macrophage function. We showed that isoproterenol concentration-dependently induced HO-1 production through β 1-but not β 2-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 β 1-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.
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