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Here we investigated the potential effect of adiponectin on NF\u2010\u03baB activation in hypertrophic neonatal rat ventricular myocytes (NRVMs) and related signal transduction pathway. We treated NRVMs with globular adiponectin (gAd) before angiotensin II (AngII) stimulation. Pretreating cells with gAd reduced the increased incorporation of [<jats:sup>3<\/jats:sup>H]\u2010leucine and the mRNA levels of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) stimulated by AngII, indicating gAd inhibited AngII\u2010induced cardiac hypertrophic signaling. Moreover, gAd pretreatment suppressed inhibitory protein \u03baB (I\u2010\u03baB) phosphorylation and decreased p65 nuclear translocation, DNA\u2010binding and transcription activity of NF\u2010\u03baB. Meanwhile, gAd promoted AMP\u2010activated protein kinase (AMPK) phosphorylation, which is a downstream signaling mediator of adiponectin. Pharmacological activator of AMPK could inhibit AngII\u2010induced NF\u2010\u03baB translocation, and inhibitor of AMPK or a dominant\u2010negative AMPK adenovirus suppressed gAd\u2010mediated inhibition of I\u2010\u03baB phosphorylation and NF\u2010\u03baB activation. When AMPK was inhibited, the suppressive effect of gAd on ANP mRNA expression was reduced. Our data indicate that gAd inhibits cardiac hypertrophic signaling through AMPK mediated suppression of NF\u2010\u03baB activation. J. Cell. Physiol. 222:149\u2013155, 2010. \u00a9 2009 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jcp.21931","type":"journal-article","created":{"date-parts":[[2009,9,24]],"date-time":"2009-09-24T17:47:25Z","timestamp":1253814445000},"page":"149-155","source":"Crossref","is-referenced-by-count":41,"title":["Globular adiponectin inhibits angiotensin II\u2010induced nuclear factor \u03baB activation through AMP\u2010activated protein kinase in cardiac 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