Effects of Conditioning with Sevoflurane before Reperfusion on Hippocampal Ischemic Injury and Insulin-like Growth Factor-1 Expression in Rats

Deng-Xin Zhang ； Kuan-Ming Chiu ； Wei-Li Wang ； Da-Peng Sun

《The Chinese Journal of Physiology》 預刊文章 Pp. 45-51

並列摘要

Sevoflurane pre-conditioning before ischemia can reduce ischemia-reperfusion injuries in cardiac, pulmonary and cerebral tissues. It is uncertain whether sevoflurane conditioning before reperfusion has similar protective effects on neuronal injuries. In this study, we explored the effect of sevoflurane conditioning (at concentrations of 1.5%, 2.4% or 3.0%) on the morphology and molecular mechanisms of the hippocampal CA1 region in male Sprague-Dawley rats subjected to global cerebral ischemia. We determined the pathological results by hematoxylin and eosin (H&E) staining and examined the mRNA levels of insulin-like growth factor-1 (IGF-1) and protein levels of p-JNK1/2 and p-Akt1 in the hippocampus at 24 h, 48 h and 72 h after global cerebral ischemia-reperfusion. Our data showed that O2 post-conditioning and lower dose (1.5%) of sevoflurane did not ameliorate ischemia-induced CA1 injury. However, higher doses of 2.4% and 3.0% sevoflurane post-conditioning alleviated the CA1 injury and enhanced the expression levels of IGF-1 mRNA. Furthermore, sevoflurane post-conditioning inhibited the activations of p-JNK1/2 and enhanced activation of p-Akt1. In conclusion, these results suggest that post-conditioning with sevoflurane at 2.4% and 3.0% ameliorates global cerebral ischemia induced hippocampal CA1 injury by up-regulating the expression of IGF-1 mRNA followed by the activation of p-Akt1 and inhibition of the activation of p-JNK1/2.

並列關鍵字

insulin-like growth factor-1 ； post-conditioning ； reperfusion injury ； sevoflurane

參考文獻

Canas, P.T.,Velly, L.J.,Labrande, C.N.,Guillet, B.A.,Sautou-Miranda, V.,Masmejean, F.M.,Nieoullon, A.L.,Gouin, F.M.,Bruder, N.J.,Pisano, P.S.(2006).Sevoflurane protects rat mixed cerebrocortical neuronal-glial cell cultures against transient oxygen-glucose deprivation: involvement of glutamate uptake and reactive oxygen species.Anesthesiology.105,990-998.

Cao, L.J.,Wang, J.,Hao, P.P.,Sun, C.L.,Chen, Y.G.(2011).Effects of ulinastatin, a urinary trypsin inhibitor, on synaptic plasticity and spatial memory in a rat model of cerebral ischemia/reperfusion injury.Chinese J. Physiol..54,435-442.

Gu, Z.,Jiang, Q.,Zhang, G.(2001).c-Jun N-terminal kinase activation in hippocampal CA1 region was involved in ischemic injury.Neuroreport.12,897-900.

Harding, T.C.,Xue, L.,Bienemann, A.,Haywood, D.,Dickens, M.,Tolkovsky, A.M.,Uney, J.B.(2001).Inhibition of JNK by overexpression of the JNL binding domain of JIP-1 prevents apoptosis in sympathetic neurons.J. Biol. Chem..276,4531-4534.

Hausenloy, D.J.,Lecour, S.,Yellon, D.M.(2011).Reperfusion injury salvage kinase and survivor activating factor enhancement prosurvival signaling pathways in ischemic postconditioning: two sides of the same coin.Antioxid. Redox Signal..14,893-907.