Effects of sevoflurane postconditioning on autophagy during focal cerebral ischemia-reperfusion in rats

Objective To evaluate the effect of sevoflurane postconditioning on autophagy during focal cerebral ischemia-reperfusion (I/R) in rats. Methods Forty-five clean-grade healthy male Sprague-Dawley rats, weighing 280-350 g, were divided into 3 groups (n=15 each) using a random number table method: sham operation group (S group), cerebral I/R group (I/R group) and sevoflurane postconditioning group (SP group). Focal cerebral I/R injury model was established by Zea-Longa method in chloral hydrate-anesthetized rats.The animals in SP group inhaled 2.4% sevoflurane for 30 min starting from onset of reperfusion.The expression of autophagy-related proteins LC3 and beclin-1 was detected by Western blot at 2 h of reperfusion.The cerebral cortex was removed for examination of the morphology and number of autophagosomes with an electron microscope.Neurological deficit was assessed and scored at 24 h of reperfusion.Rats were sacrificed at 72 h of reperfusion for determination of the cerebral infarct size. Results Compared with S group, the neurological deficit score was significantly increased, the percentage of cerebral infarct size was increased, LC3 Ⅱ/LC3 Ⅰ ratio in cerebral cortex was increased, the expression of beclin-1 was up-regulated, and the number of autophagosomes was increased in I/R and SP groups (P<0.05). Compared with I/R group, the neurological deficit score was significantly decreased, the percentage of cerebral infarct size was decreased, LC3 Ⅱ/LC3 Ⅰ ratio in cerebral cortex was decreased, the expression of beclin-1 was down-regulated, and the number of autophagosomes was reduced in SP group (P<0.05). Conclusion Sevoflurane postconditioning mitigates focal cerebral I/R injury through inhibiting autophagy in rats. Key words: Anesthetics, inhalation; Reperfusion injury; Cerebral; Autophagy