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Investigation of the effect of dietary intake of omega-3 polyunsaturated fatty acids on trauma-induced white matter injury with quantitative diffusion MRI in mice.
Journal of Neuroscience Research ( IF 4.2 ) Pub Date : 2020-08-25 , DOI: 10.1002/jnr.24705
Laura D Reyes 1, 2 , Thaddeus Haight 2, 3 , Abhishek Desai 4 , Huazhen Chen 4 , Asamoah Bosomtwi 2, 5, 6 , Alexandru Korotcov 2, 6 , Bernard Dardzinski 6 , Hee-Yong Kim 3 , Carlo Pierpaoli 1
Affiliation  

Previous studies suggest that long‐term supplementation and dietary intake of omega‐3 polyunsaturated fatty acids (PUFAs) may have neuroprotective effects following brain injury. The objective of this study was to investigate potential neuroprotective effects of omega‐3 PUFAs on white matter following closed‐head trauma. The closed‐head injury model of engineered rotational acceleration (CHIMERA) produces a reproducible injury in the optic tract and brachium of the superior colliculus in mice. Damage is detectable using diffusion tensor imaging (DTI) metrics, particularly fractional anisotropy (FA), with sensitivity comparable to histology. We acquired in vivo (n = 38) and ex vivo (n = 41) DTI data in mice divided into sham and CHIMERA groups with two dietary groups: one deficient in omega‐3 PUFAs and one adequate in omega‐3 PUFAs. We examined injury effects (reduction in FA) and neuroprotection (FA reduction modulated by diet) in the optic tract and brachium. We verified that diet did not affect FA in sham animals. In injured animals, we found significantly reduced FA in the optic tract and brachium (~10% reduction, p < 0.001), and Bayes factor analysis showed strong evidence to reject the null hypothesis. However, Bayes factor analysis showed substantial evidence to accept the null hypothesis of no diet‐related FA differences in injured animals in the in vivo and ex vivo samples. Our results indicate no neuroprotective effect from adequate dietary omega‐3 PUFA intake on white matter damage following traumatic brain injury. Since damage from CHIMERA mainly affects white matter, our results do not necessarily contradict previous findings showing omega‐3 PUFA‐mediated neuroprotection in gray matter.

中文翻译:

通过定量扩散 MRI 研究膳食摄入 omega-3 多不饱和脂肪酸对小鼠外伤诱发的白质损伤的影响。

先前的研究表明,长期补充和膳食摄入 omega-3 多不饱和脂肪酸 (PUFA) 可能在脑损伤后具有神经保护作用。本研究的目的是研究 omega-3 多不饱和脂肪酸对闭合性头部创伤后白质的潜在神经保护作用。工程旋转加速的闭合性头部损伤模型 (CHIMERA) 在小鼠的视束和上丘臂中产生可重复的损伤。使用扩散张量成像 (DTI) 指标,尤其是分数各向异性 (FA),可以检测到损伤,其灵敏度与组织学相当。我们获得了体内( n  = 38) 和体外( n = 41) 小鼠的 DTI 数据分为假组和 CHIMERA 组,有两个饮食组:一组缺乏 omega-3 多不饱和脂肪酸,另一组缺乏 omega-3 多不饱和脂肪酸。我们检查了视束和臂中的损伤效应(FA 减少)和神经保护作用(通过饮食调节 FA 减少)。我们证实饮食不会影响假手术动物的 FA。在受伤的动物中,我们发现视束和肱骨中的 FA 显着减少(减少约 10%,p  < 0.001),并且贝叶斯因子分析显示强有力的证据来拒绝原假设。然而,贝叶斯因子分析显示大量证据接受在体内体外受伤动物中没有与饮食相关的 FA 差异的原假设样品。我们的结果表明,摄入足够的 omega-3 PUFA 饮食对创伤性脑损伤后的白质损伤没有神经保护作用。由于嵌合体的损伤主要影响白质,我们的结果不一定与之前的研究结果相矛盾,该研究结果表明 omega-3 PUFA 介导的灰质神经保护作用。
更新日期:2020-10-04
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