RGD Reference Report - Delayed anesthetic preconditioning protects against myocardial infarction via activation of nuclear factor-kappaB and upregulation of autophagy. - Rat Genome Database

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Delayed anesthetic preconditioning protects against myocardial infarction via activation of nuclear factor-kappaB and upregulation of autophagy.

Authors: Qiao, S  Xie, H  Wang, C  Wu, X  Liu, H  Liu, C 
Citation: Qiao S, etal., J Anesth. 2012 Nov 10.
RGD ID: 7175553
Pubmed: PMID:23143013   (View Abstract at PubMed)
DOI: DOI:10.1007/s00540-012-1494-3   (Journal Full-text)

PURPOSE: Delayed volatile anesthetic preconditioning (APC) can protect against myocardial ischemia/reperfusion (I/R) injury; the delayed phase is called the second window of protection (SWOP), but the underlying mechanism is unclear. Nuclear factor-kappaB (NF-kappaB) is involved in the myocardial protection conferred by APC in the acute phase; autophagy has been reported to confer apoptosis inhibition and infarction reduction. We hypothesized that APC initiates delayed cardioprotection against I/R injury via the activation of NF-kB and upregulation of autophagy, thus attenuating the inflammatory response and apoptosis METHODS: After a rat I/R model was set up, left ventricular samples were obtained before I/R to assess NF-kappaB-DNA binding activity and microtubule-associated protein 1 light chain 3 (LC3) and cathepsin B protein expression, and to examine autophagosomes with a transmission electron microscope. Infarct size and the expressions of tumor necrosis factor alpha (TNF-alpha), interleukin 1beta (IL-1beta), and caspase-3 were measured at the end of 2-h reperfusion. RESULTS: The infarct size was significantly reduced in the SWOP group (30 +/- 3 %) when compared with that in the I/R group (47 +/- 7 %, P < 0.05), and this finding was associated with increased NF-kappaB-DNA binding activity and autophagosomes. In addition, the expressions of LC3-II and cathepsin B were also up-regulated, and the expressions of TNF-alpha, IL-1beta, and caspase-3 were attenuated in the SWOP group when compared with the findings in the I/R group. However, this protection was abolished by the administration of parthenolide (PTN) before sevoflurane inhalation, which resulted in an infarct size that was significantly increased (47 +/- 5 %, P < 0.05 PTN + SWOP vs. SWOP group). CONCLUSION: Delayed APC protected the rat heart from I/R injury. The underlying mechanisms may include NF-kappaB activation, upregulation of autophagy, and the attenuation of TNF-alpha, IL-1beta, and caspase-3 expressions.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
myocardial infarction  ISOIl1b (Rattus norvegicus)7175553; 7175553 RGD 
myocardial infarction  IDA 7175553 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Il1b  (interleukin 1 beta)

Genes (Mus musculus)
Il1b  (interleukin 1 beta)

Genes (Homo sapiens)
IL1B  (interleukin 1 beta)


Additional Information