Effects of conditioning with sevoflurane before reperfusion on hippocampal ischemic injury and insulin-like growth factor-1 expression in rats.

Abstract

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.

• Authors: Dengxin Zhang, Kuan-Ming Chiu, Weili Wang, Dapeng Sun
• Journal: The Chinese journal of physiology (Chin J Physiol) Vol. 56 Issue 4 Pg. 236-42 (Aug 31 2013) ISSN: 0304-4920 [Print] India
• PMID: 23806038 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Methyl Ethers
• RNA, Messenger
• Sevoflurane
• Insulin-Like Growth Factor I
• Proto-Oncogene Proteins c-akt
• JNK Mitogen-Activated Protein Kinases

Topics

• Animals
• Hippocampus (blood supply, metabolism, pathology)
• Insulin-Like Growth Factor I (genetics)
• Ischemic Postconditioning
• JNK Mitogen-Activated Protein Kinases (metabolism)
• Male
• Methyl Ethers (pharmacology)
• Proto-Oncogene Proteins c-akt (metabolism)
• RNA, Messenger (analysis)
• Rats
• Rats, Sprague-Dawley
• Reperfusion Injury (prevention & control)
• Sevoflurane