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生酮饮食可减少幼鼠创伤性脑损伤后的细胞色素c释放和细胞凋亡。

Ketogenic diet reduces cytochrome c release and cellular apoptosis following traumatic brain injury in juvenile rats.

作者信息

Hu Zhi Gang, Wang Han Dong, Jin Wei, Yin Hong Xia

机构信息

Department of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, Jiangsu, China.

出版信息

Ann Clin Lab Sci. 2009 Winter;39(1):76-83.

PMID:19201746
Abstract

Ketone bodies have been shown to be favorable alternative metabolic substrates and are protective under neuropathologies. At the same time, cytochrome c release has been reported following traumatic brain injury (TBI) and precipitates apoptosis via the mitochondrial pathway. The present study investigated the effects of a ketogenic diet (KD) on TBI. TBI was produced using the Feeney weight-drop model and the animals were fed either normal diet (ND) or KD. Brain edema was estimated by wet/dry weight ratio; cytochrome c was detected by Western blotting; cellular apoptosis in the penumbra area was examined by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) and active caspase-3 immunohistochemical staining. The results show that brain edema, cytochrome c release, and cellular apoptosis were induced after TBI and that KD reduced these changes dramatically. These findings suggest that KD has potential therapeutic benefit in TBI.

摘要

酮体已被证明是有益的替代代谢底物,并且在神经病理学情况下具有保护作用。同时,有报道称创伤性脑损伤(TBI)后会出现细胞色素c释放,并通过线粒体途径引发细胞凋亡。本研究调查了生酮饮食(KD)对TBI的影响。采用Feeney重物坠落模型制造TBI,动物分别喂食正常饮食(ND)或KD。通过湿/干重比评估脑水肿;通过蛋白质免疫印迹法检测细胞色素c;通过末端脱氧核苷酸转移酶介导的dUTP缺口末端标记(TUNEL)和活性半胱天冬酶-3免疫组织化学染色检查半暗带区域的细胞凋亡。结果表明,TBI后会诱导脑水肿、细胞色素c释放和细胞凋亡,而KD可显著减轻这些变化。这些发现表明,KD对TBI具有潜在的治疗益处。

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