期刊
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
卷 30, 期 3, 页码 616-627出版社
SAGE PUBLICATIONS INC
DOI: 10.1038/jcbfm.2009.234
关键词
Bad; Bcl-xL; caspase-3; cytochrome c; neuroprotection
资金
- ISF [241/04]
Heat acclimation (HA) offers functional neuroprotection in mice after traumatic brain injury (TBI). This study further characterizes endogenous neuroprotection acquired by HA (34 +/- 1 degrees C, 30 d) after TBI. We establish here the ability of HA to induce sustained functional benefits and to reduce activation of apoptotic pathways. Neurobehavioral recovery, assessed by the Neurological Severity Score, was greater in HA mice up to 8 days after injury as compared with normothermic controls (P < 0.05) and lesion volume was also smaller in the HA group (P < 0.05). Reduced apoptotic cell death in HA mice was confirmed using caspase-3 activity measurements and immunohistochemistry. To investigate the underlying molecular pathways, expression levels of intrinsic apoptotic pathway-related proteins were examined. HA mice displayed higher mitochondrial levels of antiapoptotic Bcl-xL, accompanied by lower proapoptotic Bad levels and decreased cytochrome c release, suggesting a higher apoptotic threshold. Taken together with our previous reports, indicating increased Akt phosphorylation and antioxidative capacity, alongside with reduced tumor necrosis alpha levels after TBI in HA animals, the current results support the involvement of an antiapoptotic effect in HA-induced neuroprotection. Current results warrant further study as TBI-induced apoptosis may persist over weeks after injury, possibly providing a target for belated therapeutic intervention. Journal of Cerebral Blood Flow & Metabolism (2010) 30, 616-627; doi: 10.1038/jcbfm.2009.234; published online 11 November 2009
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据