RGD Reference Report - Roles of TNF-alpha and its receptors in the beneficial effects of vagal stimulation after myocardial infarction in rats. - Rat Genome Database

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Roles of TNF-alpha and its receptors in the beneficial effects of vagal stimulation after myocardial infarction in rats.

Authors: Kong, SS  Liu, JJ  Hwang, TC  Yu, XJ  Lu, Y  Zang, WJ 
Citation: Kong SS, etal., Clin Exp Pharmacol Physiol. 2011 Mar 1. doi: 10.1111/j.1440-1681.2011.05505.x.
RGD ID: 5130892
Pubmed: PMID:21362018   (View Abstract at PubMed)
DOI: DOI:10.1111/j.1440-1681.2011.05505.x   (Journal Full-text)

Acute myocardial infarction (AMI) often activates the sympathetic system and inhibits the vagal system. Long-term vagal nerve stimulation (VNS) exerts several beneficial effects on the ischemia heart including an anti-inflammatory effect. The goal of the current study is to investigate, in a rodent model, whether short term VNS during AMI could inhibit the expression of tumor necrosis factor-alpha (TNF-alpha) and the effect of TNF receptor (TNFR), key components in inflammatory responses to AMI. Adult male Sprague-Dawley rats were divided into four groups: control (C), vagal nerve stimulation (S), acute myocardial infarction (M), pre-VNS(+) AMI (MS). The right vagus nerve was electrically stimulated for 4 hours. The hemodynamic data were continuously monitored by a multichannel physiologic recorder. Lactate dehydrogenase (LDH) leakage and creatine kinase (CK) as well as infarct size were measured. The expression of TNF-alpha and its receptor were analyzed by reverse transcription polymerase chain reaction (RT-PCR), Western blotting and enzyme-linked immunosorbent assay (ELISA). In M group, AMI rats presented low blood pressure, high left ventricular end-diastolic pressure, a depressed maximum dP/dt of left ventricular pressure, higher LDH and CK leakage and larger infarct size as well as an increased TNF-alpha level and increased TNFR1/TNFR2 ratio. However, these presumably harmful effects of AMI were all significantly ameliorated by VNS during AMI. In conclusion, VNS can rectify ischemia-induced cardiac dysfunction partly through an inhibitory effect of VNS on the TNF-alpha-mediated signaling pathway.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
myocardial infarction  ISOTnf (Rattus norvegicus)5130892; 5130892mRNA more ...RGD 
myocardial infarction  ISOTnfrsf1a (Rattus norvegicus)5130892; 5130892mRNA and protein:increased expression:left ventricle myocardium (rat)RGD 
myocardial infarction  ISOTnfrsf1b (Rattus norvegicus)5130892; 5130892mRNA and protein:decreased expression:left ventricle myocardium (rat)RGD 
myocardial infarction  IEP 5130892mRNA more ...RGD 
myocardial infarction  IEP 5130892mRNA and protein:increased expression:left ventricle myocardium (rat)RGD 
myocardial infarction  IEP 5130892mRNA and protein:decreased expression:left ventricle myocardium (rat)RGD 

Objects Annotated

Genes (Rattus norvegicus)
Tnf  (tumor necrosis factor)
Tnfrsf1a  (TNF receptor superfamily member 1A)
Tnfrsf1b  (TNF receptor superfamily member 1B)

Genes (Mus musculus)
Tnf  (tumor necrosis factor)
Tnfrsf1a  (tumor necrosis factor receptor superfamily, member 1a)
Tnfrsf1b  (tumor necrosis factor receptor superfamily, member 1b)

Genes (Homo sapiens)
TNF  (tumor necrosis factor)
TNFRSF1A  (TNF receptor superfamily member 1A)
TNFRSF1B  (TNF receptor superfamily member 1B)


Additional Information