Journal
EVIDENCE-BASED COMPLEMENTARY AND ALTERNATIVE MEDICINE
Volume 7, Issue 1, Pages 63-68Publisher
HINDAWI LTD
DOI: 10.1093/ecam/nem146
Keywords
adenosine A(2A) receptor; 5-bromodeoxy uridine; neuronal differentiation; neurotrophic factor
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Earlier we identified adenosine monophosphate (AMP) N-1-oxide as a unique compound of royal jelly (RJ) that induces neurite outgrowth (neuritegenesis) from cultured rat pheochromocytoma PC12 cells via the adenosine A(2A) receptor. Now, we found that AMP N-1-oxide stimulated the phosphorylation of not only mitogen-activated protein kinase (MAPK) but also that of cAMP/calcium-response element-binding protein (CREB) in a dose-dependent manner. Inhibition of MAPK activation by a MEK inhibitor, PD98059, did not influence the AMP N-1-oxide-induced neuritegenesis, whereas that of protein kinase A (PKA) by a selective inhibitor, KT5720, significantly reduced neurite outgrowth. AMP N-1-oxide also had the activity of suppressing the growth of PC12 cells, which correlated well with the neurite outgrowth-promoting activity. KT5720 restored the growth of AMP N-1-oxide-treated PC12 cells. It is well known that nerve growth factor suppresses proliferation of PC12 cells before causing stimulation of neuronal differentiation. Thus, AMP N-1-oxide elicited neuronal differentiation of PC12 cells, as evidenced by generation of neurites, and inhibited cell growth through adenosine A(2A) receptor-mediated PKA signaling, which may be responsible for characteristic actions of RJ.
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