Abstract：Objective: To explore the effects of sevoflurane on cerebral ischemia-reperfusion injury in rats and its mechanism. Methods: SD rats were randomly divided into sham operation group (Sham), ischemia-reperfusion injury group (I/R), ischemia-reperfusion injury+sevoflurane group (I/R+Sev) and ischemia-reperfusion injury+sevoflurane+EX527 group (I/R+Sev+EX527). Morris Water Maze test and TTC staining were used to observe the cerebral ischemia reperfusion injury. The apoptosis of nerve cells was detected by TUNEL staining. Transmission electron microscopy was used to detect autophagy. Western blotting was used to detect the expression of autophagy, apoptosis-related proteins and SIRT1-FOXO1 pathway proteins. Results: Compared with the sham group, the escape latency of rats in the I/R group was prolonged, the number of crossing the platform was decreased, the volume of cerebral infarction was significantly increased, the rate of neuronal apoptosis was significantly increased, and the number of autophagic vacuoles was significantly increased. The expression of Bad, cleaved-caspase-3, LC3-II/I protein were increased significantly, the expression of Bcl-2, p62, SIRT1, FOXO1 protein were decreased significantly, and the differences were statistically significant (P<0.05). Compared with the I/R group, the escape latency of rats in the I/R+Sev group was reduced, the number of crossing the platform was increased, the volume of cerebral infarction was significantly decreased, the rate of neuronal apoptosis was significantly decreased, and the number of autophagic vacuoles was significantly decreased. The expression of Bad, Cleaved-caspase-3, LC3-II/I was significantly decreased, and the protein expressions of Bcl-2, p62, SIRT1 and FOXO1 were significantly increased, and the differences were statistically significant (P<0.05). Compared with the I/R+Sev group, the escape latency of the I/R+Sev+EX527 group was prolonged, the number of crossing the platform was decreased, the volume of cerebral infarction was increased, the rate of neuronal apoptosis was increased, and the number of autophagic vacuoles was increased. The expression of cleaved-caspase-3, LC3-II/I protein were increased, and the protein expression of Bcl-2, p62, SIRT1, FOXO1 were decreased, and the differences were statistically significant (P<0.05). Conclusion: Sevoflurane treatment may protect rats from cerebral ischemia-reperfusion injury by inhibiting autophagy and apoptosis by a mechanism related to the SIRT1-FOXO1 signalling pathway.
陈健, 李成洁, 李媛. 七氟醚可能通过调控SIRT1-FOXO1介导的自噬对大鼠脑缺血再灌注损伤的影响[J]. 河北医学, 2022, 28(3): 374-379.
CHEN Jian, LI Chengjie, et al. Effects of Sevoflurane on Cerebral Ischemia-Reperfusion Injury in Rats Possibly Through Modulation of SIRT1-FOXO1-Mediated Autophagy. HeBei Med, 2022, 28(3): 374-379.
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2022, Vol. 28 
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