Clostridium butyricum pretreatment attenuates cerebral ischemia/reperfusion injury in mice via anti-oxidation and anti-apoptosis. (2nd February 2016)

• Record Type: Journal Article
• Authors: Sun, Jing; Ling, Zongxin; Wang, Fangyan; Chen, Wenqian; Li, Haixiao; Jin, Jiangtao; Zhang, Huiqing; Pang, Mengqi; Yu, Junjie; Liu, Jiaming
• Is Part Of: Neuroscience letters. Volume 613(2016)
• Page Start: 30
• Page End: 35
• Publication Date: 2016-02-02
• Subjects: Cerebral ischemic/reperfusion injury -- Anti-oxidative -- Anti-apoptosis -- Neuroprotective effects -- Butyrate; Neurology -- Periodicals; Neurology -- Periodicals; Research -- Periodicals; Neurologie -- Périodiques; Neuroanatomie -- Périodiques; Neuropharmacologie -- Périodiques; Neurophysiologie -- Périodiques; Neurology; Periodicals; Electronic journals; 617.48
• DOI: 10.1016/j.neulet.2015.12.047
• Languages: English
• ISSNs: 0304-3940

Abstract

Highlights: C. butyricum attenuates cerebral ischemia/reperfusion injury in the I/R mice. C. butyricum ameliorate neurological deficit in the I/R mice. C. butyricum exerts protective effects via anti-oxidative and anti-apoptosis. A butyrate might be involved in the neuroprotective effects of C. butyricum . Abstract: Probiotics participate actively in the neuropsychiatric disorders. However, their roles on ischemic stroke remain unclear. This study aims to determine whether Clostridium butyricum ( C. butyricum ) could attenuate cerebral ischemia/reperfusion (I/R) injury and its possible mechanisms. Male ICR mice were intragastrically pretreated with C. butyricum for 2 successive weeks, and then subjected to cerebral I/R injury induced by the bilateral common carotid artery occlusion (BCCAO) for 20 min. After 24 h of the reperfusion, neurological deficit scores were evaluated. Histopathological changes of the hippocampus neurons were observed using Hematoxylin and eosin (H&E) and TUNEL staining. Malondialdehyde (MDA) contents and superoxide dismutase (SOD) activities in the brain were detected. The expression of Caspase-3, Bax and Bcl-2 were investigated by Western blot and immunohistochemistry analysis. The butyrate contents in the brain were determined. Our results showed that cerebral I/R injury led to neurological deficit, increased levels of Caspase-3 and Bax and decreased Bcl-2/Bax ratio. C. butyricum significantly improved neurological deficit, relieved histopathologic change, decreased MDA contents and increased SOD activities in the I/R injury mice. After C. butyricum pretreatment, the expression of Caspase-3 and Bax were significantly decreased, the Bcl-2/Bax ratio was significantly increased, and butyrate contents in the brain were significantly increased. These findings suggested that C. butyricum is able to exert neuroprotective effects against I/R injury mice through anti-oxidant and anti-apoptotic mechanisms, and reversing decrease of butyrate contents in the brain might be involved in its neuroprotection.