RGD Reference Report - Activation of NF-kappaB is a critical element in the antiapoptotic effect of anesthetic preconditioning. - Rat Genome Database

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Activation of NF-kappaB is a critical element in the antiapoptotic effect of anesthetic preconditioning.

Authors: Lu, X  Liu, H  Wang, L  Schaefer, S 
Citation: Lu X, etal., Am J Physiol Heart Circ Physiol. 2009 May;296(5):H1296-304. doi: 10.1152/ajpheart.01282.2008. Epub 2009 Mar 20.
RGD ID: 10413871
Pubmed: PMID:19304943   (View Abstract at PubMed)
DOI: DOI:10.1152/ajpheart.01282.2008   (Journal Full-text)

Anesthetic preconditioning (APC), defined as brief exposure to inhalational anesthetics before cardiac ischemia-reperfusion (I/R), limits injury in both animal models and in humans. APC can result in the production of reactive oxygen species (ROS), and prior work has shown that APC can modify activation of NF-kappaB during I/R, with consequent reduction in the expression of inflammatory mediators. However, the role of NF-kappaB activation before I/R is unknown. Therefore, these experiments tested the hypothesis that APC-induced ROS results in activation of NF-kappaB before I/R, with consequent increased expression of antiapoptotic proteins such as Bcl-2 and decreased apoptosis. Experiments utilized an established perfused heart rat model of sevoflurane APC and I/R. The role of NF-kappaB was defined by a novel method of transient inhibition of the regulatory kinase IKK using the reversible inhibitor SC-514. In addition to functional measures of left ventricular developed and end-diastolic pressure, phosphorylation of IkappaBalpha and activation of NF-kappaB were measured along with cytosolic protein content of Bcl-2, release of cytochrome c, and degradation of caspase-3. APC resulted in ROS-dependent phosphorylation of IkappaBalpha and activation of NF-kappaB before I/R. APC also increased the expression of Bcl-2 before I/R. In addition to functional protection following I/R, APC resulted in lower release of cytochrome c and caspase-3 degradation. These protective effects of APC were abolished by transient inhibition of IkappaBalpha phosphorylation and NF-kappaB activation by SC-514 followed by washout. ROS-dependent activation of NF-kappaB by APC before I/R is a critical element in the protective effect of APC. APC reduces apoptosis and functional impairment by increasing Bcl-2 expression before I/R. Interventions that increase NF-kappaB activation before I/R should protect hearts from I/R injury.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
NFKBIAHumanMyocardial Reperfusion Injury treatmentISONfkbia (Rattus norvegicus) RGD 
NfkbiaRatMyocardial Reperfusion Injury treatmentIDA  RGD 
NfkbiaMouseMyocardial Reperfusion Injury treatmentISONfkbia (Rattus norvegicus) RGD 

Objects Annotated

Genes (Rattus norvegicus)
Nfkbia  (NFKB inhibitor alpha)

Genes (Mus musculus)
Nfkbia  (nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha)

Genes (Homo sapiens)
NFKBIA  (NFKB inhibitor alpha)


Additional Information