ω-3脂肪酸和维生素D可降低实验性创伤性脑损伤中的血浆总tau蛋白、胶质纤维酸性蛋白和泛素羧基末端水解酶L1水平。
Omega-3 Fatty Acids and Vitamin D Decrease Plasma T-Tau, GFAP, and UCH-L1 in Experimental Traumatic Brain Injury.
作者信息
Scrimgeour Angus G, Condlin Michelle L, Loban Andrei, DeMar James C
机构信息
Military Nutrition Division, US Army Research Institute of Environmental Medicine, Natick, MA, United States.
Blast-Induced Neurotrauma Branch, Center for Military Psychiatry and Neuroscience Research, Walter Reed Army Institute of Research (WRAIR), Silver Spring, MD, United States.
出版信息
Front Nutr. 2021 Jun 4;8:685220. doi: 10.3389/fnut.2021.685220. eCollection 2021.
Traumatic brain injury (TBI) results in neuronal, axonal and glial damage. Interventions targeting neuroinflammation to enhance recovery from TBI are needed. Exercise is known to improve cognitive function in TBI patients. Omega-3 fatty acids and vitamin D reportedly reduce inflammation, and in combination, might improve TBI outcomes. This study examined how an anti-inflammatory diet affected plasma TBI biomarkers, voluntary exercise and behaviors following exposure to mild TBI (mTBI). Adult, male rats were individually housed in cages fitted with running wheels and daily running distance was recorded throughout the study. A modified weight drop method induced mTBI, and during 30 days post-injury, rats were fed diets supplemented with omega-3 fatty acids and vitamin D (AIDM diet), or non-supplemented AIN-76A diets (CON diet). Behavioral tests were periodically conducted to assess functional deficits. Plasma levels of Total tau (T-tau), glial fibrillary acidic protein (GFAP), ubiquitin c-terminal hydrolase L1 (UCH-L1) and neurofilament light chain (NF-L) were measured at 48 h, 14 days, and 30 days post-injury. Fatty acid composition of food, plasma, and brain tissues was determined. In rats exposed to mTBI, NF-L levels were significantly elevated at 48 h post-injury ( < 0.005), and decreased to levels seen in uninjured rats by 14 days post-injury. T-tau, GFAP, and UCH-L1 plasma levels did not change at 48 h or 14 days post-injury. However, at 30 days post-injury, T-tau, GFAP and UCH-L1 all significantly increased in rats exposed to mTBI and fed CON diets ( < 0.005), but not in rats fed AIDM diets. Behavioral tests conducted post-injury showed that exercise counteracted cognitive deficits associated with mTBI. The AIDM diets significantly increased docosahexaenoic acid levels in plasma and brain tissue ( < 0.05), and in serum levels of vitamin D ( < 0.05). The temporal response of the four injury biomarkers examined is consistent with studies by others demonstrating acute and chronic neural tissue damage following exposure to TBI. The anti-inflammatory diet significantly altered the temporal profiles of plasma T-tau, GFAP, and UCH-L1 following mTBI. Voluntary exercise protected against mTBI-induced cognitive deficits, but had no impact on plasma levels of neurotrauma biomarkers. Thus, the prophylactic effect of exercise, when combined with an anti-inflammatory diet, may facilitate recovery in patients with mTBI.
创伤性脑损伤(TBI)会导致神经元、轴突和神经胶质损伤。需要针对神经炎症进行干预以促进TBI后的恢复。已知运动可改善TBI患者的认知功能。据报道,ω-3脂肪酸和维生素D可减轻炎症,两者联合使用可能会改善TBI的预后。本研究探讨了抗炎饮食对轻度创伤性脑损伤(mTBI)后血浆TBI生物标志物、自主运动和行为的影响。成年雄性大鼠单独饲养在装有跑步轮的笼子里,在整个研究过程中记录每日跑步距离。采用改良的重物坠落法诱导mTBI,在损伤后的30天内,给大鼠喂食补充了ω-3脂肪酸和维生素D的饮食(AIDM饮食),或未补充的AIN-76A饮食(CON饮食)。定期进行行为测试以评估功能缺陷。在损伤后48小时、14天和30天测量血浆总tau蛋白(T-tau)、胶质纤维酸性蛋白(GFAP)、泛素C末端水解酶L1(UCH-L1)和神经丝轻链(NF-L)的水平。测定食物、血浆和脑组织的脂肪酸组成。在暴露于mTBI的大鼠中,损伤后48小时NF-L水平显著升高(<0.005),损伤后14天降至未受伤大鼠的水平。损伤后48小时或14天,T-tau、GFAP和UCH-L1的血浆水平没有变化。然而,在损伤后30天,暴露于mTBI并喂食CON饮食的大鼠中,T-tau、GFAP和UCH-L1均显著升高(<0.005),而喂食AIDM饮食的大鼠则没有。损伤后进行的行为测试表明,运动可抵消与mTBI相关的认知缺陷。AIDM饮食显著提高了血浆和脑组织中二十二碳六烯酸的水平(<0.05),以及血清中维生素D的水平(<0.05)。所检测的四种损伤生物标志物的时间反应与其他研究一致,这些研究表明暴露于TBI后会出现急性和慢性神经组织损伤。抗炎饮食显著改变了mTBI后血浆T-tau、GFAP和UCH-L1的时间变化曲线。自主运动可预防mTBI诱导的认知缺陷,但对神经创伤生物标志物的血浆水平没有影响。因此,运动与抗炎饮食相结合的预防作用可能有助于mTBI患者的恢复。
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