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Sevoflurane postconditioning against cerebral ischemic neuronal injury is abolished in diet-induced obesity: Role of brain mitochondrial KATP channels

  • Authors:
    • Zecheng Yang
    • Yunbo Chen
    • Yan Zhang
    • Yi Jiang
    • Xuedong Fang
    • Jingwei Xu

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  • Published online on: January 22, 2014     https://doi.org/10.3892/mmr.2014.1912
  • Pages: 843-850
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
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Abstract

Obesity is associated with increased infarct volumes and adverse outcomes following ischemic stroke. However, its effect on anesthetic postconditioning‑induced neuroprotection has not been investigated. The present study examined the effect of sevoflurane postconditioning on focal ischemic brain injury in diet‑induced obesity. Sprague‑Dawley rats were fed a high‑fat diet (HF; 45% kcal as fat) for 12 weeks to develop obesity syndrome. Rats fed a low‑fat diet (LF; 10% kcal as fat) served as controls. The HF or LF‑fed rats were subjected to focal cerebral ischemia for 60 min, followed by 24 h of reperfusion. Postconditioning was performed by exposure to sevoflurane for 15 min immediately at the onset of reperfusion. The involvement of the mitochondrial KATP (mitoKATP) channel was analyzed by the administration of a selective inhibitor of 5‑hydroxydecanoate (5‑HD) prior to sevoflurane postconditioning or by administration of diazoxide (DZX), a mitoKATP channel opener, instead of sevoflurane. The cerebral infarct volume, neurological score and motor coordination were evaluated 24 h after reperfusion. The HF‑fed rats had larger infarct volumes, and lower neurological scores than the LF‑fed rats and also failed to respond to neuroprotection by sevoflurane or DZX. By contrast, sevoflurane and DZX reduced the infarct volumes and improved the neurological scores and motor coordination in the LF‑fed rats. Pretreatment with 5‑HD inhibited sevoflurane‑induced neuroprotection in the LF‑fed rats, whereas it had no effect in the HF‑fed rats. Molecular studies demonstrated that the expression of Kir6.2, a significant mitoKATP channel component, was reduced in the brains of the HF‑fed rats compared with the LF‑fed rats. The results of this study indicate that diet‑induced obesity eliminates the ability of anesthetic sevoflurane postconditioning to protect the brain against cerebral ischemic neuronal injury, most likely due to an impaired brain mitoKATP channel.
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2014-March
Volume 9 Issue 3

Print ISSN: 1791-2997
Online ISSN:1791-3004

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  • Journal Metrics
  • Impact Factor: 3.4
  • Ranked Medicine Research and Experimental
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  • CiteScore: 6.9
  • CiteScore Rank: Q2: #98/328 Biochemistry, Genetics and Molecular Biology
  • Source Normalized Impact per Paper (SNIP): 0.721
  • SCImago Journal Rank (SJR): 0.65
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Spandidos Publications style
Yang Z, Chen Y, Zhang Y, Jiang Y, Fang X and Xu J: Sevoflurane postconditioning against cerebral ischemic neuronal injury is abolished in diet-induced obesity: Role of brain mitochondrial KATP channels. Mol Med Rep 9: 843-850, 2014
APA
Yang, Z., Chen, Y., Zhang, Y., Jiang, Y., Fang, X., & Xu, J. (2014). Sevoflurane postconditioning against cerebral ischemic neuronal injury is abolished in diet-induced obesity: Role of brain mitochondrial KATP channels. Molecular Medicine Reports, 9, 843-850. https://doi.org/10.3892/mmr.2014.1912
MLA
Yang, Z., Chen, Y., Zhang, Y., Jiang, Y., Fang, X., Xu, J."Sevoflurane postconditioning against cerebral ischemic neuronal injury is abolished in diet-induced obesity: Role of brain mitochondrial KATP channels". Molecular Medicine Reports 9.3 (2014): 843-850.
Chicago
Yang, Z., Chen, Y., Zhang, Y., Jiang, Y., Fang, X., Xu, J."Sevoflurane postconditioning against cerebral ischemic neuronal injury is abolished in diet-induced obesity: Role of brain mitochondrial KATP channels". Molecular Medicine Reports 9, no. 3 (2014): 843-850. https://doi.org/10.3892/mmr.2014.1912