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Biomed Res Int. 2015;2015:395895. doi: 10.1155/2015/395895. Epub 2015 May 7.

Neuroprotective Effect of Sodium Butyrate against Cerebral Ischemia/Reperfusion Injury in Mice.

Author information

1
Department of Neurology, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215004, China ; Department of Neurology, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325027, China.
2
School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang 325035, China.
3
School of Environmental Science and Public Health, Wenzhou Medical University, Wenzhou, Zhejiang 325035, China.
4
Department of Neurology, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215004, China.

Abstract

Sodium butyrate (NaB) is a dietary microbial fermentation product of fiber and serves as an important neuromodulator in the central nervous system. In this study, we further investigated that NaB attenuated cerebral ischemia/reperfusion (I/R) injury in vivo and its possible mechanisms. NaB (5, 10 mg/kg) was administered intragastrically 3 h after the onset of reperfusion in bilateral common carotid artery occlusion (BCCAO) mice. After 24 h of reperfusion, neurological deficits scores were estimated. Morphological examination was performed by electron microscopy and hematoxylin-eosin (H&E) staining. The levels of oxidative stress and inflammatory cytokines were assessed. Apoptotic neurons were measured by TUNEL; apoptosis-related protein caspase-3, Bcl-2, Bax, the phosphorylation Akt (p-Akt), and BDNF were assayed by western blot and immunohistochemistry. The results showed that 10 mg/kg NaB treatment significantly ameliorated neurological deficit and histopathology changes in cerebral I/R injury. Moreover, 10 mg/kg NaB treatment markedly restored the levels of MDA, SOD, IL-1β, TNF-α, and IL-8. 10 mg/kg NaB treatment also remarkably inhibited the apoptosis, decreasing the levels of caspase-3 and Bax and increasing the levels of Bcl-2, p-Akt, and BDNF. This study suggested that NaB exerts neuroprotective effects on cerebral I/R injury by antioxidant, anti-inflammatory, and antiapoptotic properties and BDNF-PI3K/Akt pathway is involved in antiapoptotic effect.

PMID:
26064905
PMCID:
PMC4439479
DOI:
10.1155/2015/395895
[Indexed for MEDLINE]
Free PMC Article

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