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饮食摄入会改变经历过脑震荡的幼鼠大脑中的行为恢复和基因表达谱。

Dietary intake alters behavioral recovery and gene expression profiles in the brain of juvenile rats that have experienced a concussion.

作者信息

Mychasiuk Richelle, Hehar Harleen, Ma Irene, Esser Michael J

机构信息

Faculty of Medicine, Alberta Children's Hospital Research Institute, University of Calgary Calgary, AB, Canada.

出版信息

Front Behav Neurosci. 2015 Feb 5;9:17. doi: 10.3389/fnbeh.2015.00017. eCollection 2015.

DOI:10.3389/fnbeh.2015.00017
PMID:25698949
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4318392/
Abstract

Concussion and mild traumatic brain injury (mTBI) research has made minimal progress diagnosing who will suffer from lingering symptomology or generating effective treatment strategies. Research demonstrates that dietary intake affects many biological systems including brain and neurological health. This study determined if exposure to a high fat diet (HFD) or caloric restriction (CR) altered post-concussion susceptibility or resiliency using a rodent model of pediatric concussion. Rats were maintained on HFD, CR, or standard diet (STD) throughout life (including the prenatal period and weaning). At postnatal day 30, male and female rats experienced a concussion or a sham injury which was followed by 17 days of testing. Prefrontal cortex and hippocampus tissue was collected for molecular profiling. Gene expression changes in BDNF, CREB, DNMT1, FGF-2, IGF1, LEP, PGC-1α, SIRT1, Tau, and TERT were analyzed with respect to injury and diet. Analysis of telomere length (TL) using peripheral skin cells and brain tissue found that TL in skin significantly correlated with TL in brain tissue and TL was affected by dietary intake and injury status. With respect to mTBI outcomes, diet was correlated with recovery as animals on the HFD often displayed poorer performance than animals on the CR diet. Molecular analysis demonstrated that diet induced epigenetic changes that can be associated with differences in individual predisposition and resiliency to post-concussion syndrome.

摘要

脑震荡和轻度创伤性脑损伤(mTBI)的研究在诊断哪些人会出现持续症状或制定有效治疗策略方面进展甚微。研究表明,饮食摄入会影响包括大脑和神经健康在内的许多生物系统。本研究使用小儿脑震荡的啮齿动物模型,确定高脂肪饮食(HFD)或热量限制(CR)是否会改变脑震荡后的易感性或恢复力。大鼠在整个生命过程中(包括孕期和断奶期)维持HFD、CR或标准饮食(STD)。在出生后第30天,雄性和雌性大鼠经历脑震荡或假损伤,随后进行17天的测试。收集前额叶皮层和海马组织进行分子分析。分析了脑源性神经营养因子(BDNF)、环磷腺苷效应元件结合蛋白(CREB)、DNA甲基转移酶1(DNMT1)、成纤维细胞生长因子2(FGF-2)、胰岛素样生长因子1(IGF1)、瘦素(LEP)、过氧化物酶体增殖物激活受体γ共激活因子1α(PGC-1α)、沉默信息调节因子1(SIRT1)、微管相关蛋白tau(Tau)和端粒酶逆转录酶(TERT)在损伤和饮食方面的基因表达变化。使用外周皮肤细胞和脑组织分析端粒长度(TL)发现,皮肤中的TL与脑组织中的TL显著相关,且TL受饮食摄入和损伤状态的影响。关于mTBI的结果,饮食与恢复相关,因为HFD组的动物通常比CR饮食组的动物表现更差。分子分析表明,饮食诱导了表观遗传变化,这可能与个体对脑震荡后综合征的易感性和恢复力差异有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4327/4318392/70f0fb188b3e/fnbeh-09-00017-g0010.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4327/4318392/ad248c5416c0/fnbeh-09-00017-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4327/4318392/f849cdb8933c/fnbeh-09-00017-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4327/4318392/634e65ce6564/fnbeh-09-00017-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4327/4318392/d7df09fef451/fnbeh-09-00017-g0007.jpg
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