RGD Reference Report - Dobutamine-mediated heme oxygenase-1 induction via PI3K and p38 MAPK inhibits high mobility group box 1 protein release and attenuates rat myocardial ischemia/reperfusion injury in vivo.

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Dobutamine-mediated heme oxygenase-1 induction via PI3K and p38 MAPK inhibits high mobility group box 1 protein release and attenuates rat myocardial ischemia/reperfusion injury in vivo.
Authors:	Wang, J Yang, H Hu, X Fu, W Xie, J Zhou, X Xu, W Jiang, H
Citation:	Wang J, etal., J Surg Res. 2013 Aug;183(2):509-16. doi: 10.1016/j.jss.2013.02.051. Epub 2013 Mar 17.
RGD ID:	10402066
Pubmed:	PMID:23531454 (View Abstract at PubMed)
DOI:	DOI:10.1016/j.jss.2013.02.051 (Journal Full-text)
BACKGROUND: It has been reported that the induction of heme oxygenase-1 (HO-1) mediated by beta1-adrenergic receptor inhibits high mobility group box 1 protein (HMGB1) release and increases the survival rate in cecal ligation and puncture-induced septic mice. The present study aimed to investigate whether dobutamine, a selective beta1-adrenergic receptor agonist, could inhibit HMGB1 release via beta1-adrenergic receptor-mediated HO-1 induction and attenuate myocardial ischemia/reperfusion (I/R) injury in rats. MATERIALS AND METHODS: Anesthetized male rats were pretreated with dobutamine (5 or 10 mug. Kg-1. min-1, intravenous) before ischemia in the absence and/or presence of LY294002 (0.3 mg/Kg), a phosphatidylinositol 3-kinase (PI3K)< inhibitor; SB203580 (1 mg/Kg), a p38 mitogen-activated-protein kinase (P38 mitogen-activated-protein kinase [p38 MAPK]) inhibitor, and zinc protoporphyrin IX ([ZnPPIX], 10 mg/Kg), a HO-1 inhibitor, respectively, and then subjected to ischemia for 30 min followed by reperfusion for 4 h. The myocardial I/R injury and oxidative stress were assessed. Likewise, the expressions of HO-1 protein, nuclear factor kappa B (NF-kappaB) p65, and HMGB1 were measured by Western blot analysis. RESULTS: Dobutamine significantly and dose-dependently attenuated myocardial I/R injury, reduced oxidative stress, and caused the induction of HO-1, the reduction of NF-kappaB activation and HMGB1 over expression. However, all the effects caused by dobutamine were significantly reversed by the presence of LY294002, SB203580, and ZnPPIX, respectively. CONCLUSIONS: The present study demonstrated that dobutamine mediated the induction of HO-1 by selectively stimulating beta1-adrenergic receptor via PI3K and p38 MAPK, which inhibited HMGB1 release and attenuated rat myocardial I/R injury in vivo.

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Object Symbol	Species	Term	Qualifier	Evidence	With	Notes	Source	Original Reference(s)
HMGB1	Human	Myocardial Reperfusion Injury	treatment	ISO	Hmgb1 (Rattus norvegicus)		RGD
Hmgb1	Rat	Myocardial Reperfusion Injury	treatment	IEP			RGD
Hmgb1	Mouse	Myocardial Reperfusion Injury	treatment	ISO	Hmgb1 (Rattus norvegicus)		RGD

Objects Annotated

Genes (Rattus norvegicus)

Hmgb1 (high mobility group box 1)

Genes (Mus musculus)

Hmgb1 (high mobility group box 1)

Genes (Homo sapiens)

HMGB1 (high mobility group box 1)

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Dobutamine-mediated heme oxygenase-1 induction via PI3K and p38 MAPK inhibits high mobility group box 1 protein release and attenuates rat myocardial ischemia/reperfusion injury in vivo.