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

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