1University of California at Los Angeles, Los Angeles, CA, USA.
Neurorehabil Neural Repair. 2014 Jan;28(1):75-84. doi: 10.1177/1545968313498650. Epub 2013 Aug 1.
Damage to the plasma membrane is a prevalent but often neglected aspect of traumatic brain injury (TBI), which can impair neuronal signaling and hamper neurological recovery.
This study was performed to assess a new noninvasive intervention to counteract peroxidative damage to the phospholipids in the membrane using the powerful action of foods. Although dietary docosahexaenoic acid (C22:6n-3; DHA) provides protection against TBI, the pervasive effects of TBI that cause phospholipid damage, including to DHA, raises concerns about how to preserve DHA in the brain for optimal functional recovery.
Rats were maintained on curcumin and/or DHA-enriched diets for 2 weeks postinjury, and their brains were subjected to analyses.
Fluid percussion injury reduced DHA levels as well as levels of enzymes involved in the metabolism of DHA such as FADS2 and 17β-HSD4 and elevated levels of markers of lipid peroxidation such as 4-hydroxy-2-nonenal (4-HNE) and 4-hydroxy-2-hexenal (4-HHE). These effects were counteracted by DHA or curcumin, whereas the combination of curcumin and DHA had an enhanced effect on DHA and 4-HNE. The combination of curcumin and DHA was also efficient in counteracting reductions in the plasticity markers, brain-derived neurotrophic factor and its receptor p-trkB, and learning ability, which had been lessened after TBI.
Curcumin complements the action of DHA on TBI pathology, and this property appears to be a viable strategy to counteract neuronal dysfunction after TBI and complement the application of rehabilitative interventions to foster functional recovery.
细胞膜损伤是创伤性脑损伤（TBI）中普遍存在但常被忽视的一个方面，它会损害神经元信号传递并阻碍神经恢复。
本研究旨在评估一种新的非侵入性干预措施，以利用食物的强大作用来对抗膜中磷脂的过氧化损伤。尽管膳食二十二碳六烯酸（C22:6n-3；DHA）可提供针对 TBI 的保护，但 TBI 造成的普遍影响会导致磷脂损伤，包括 DHA，这引发了如何在大脑中保留 DHA 以实现最佳功能恢复的问题。
大鼠在损伤后 2 周内维持在姜黄素和/或富含 DHA 的饮食中，然后对其大脑进行分析。
流体冲击损伤降低了 DHA 水平以及参与 DHA 代谢的酶如 FADS2 和 17β-HSD4 的水平，并升高了脂质过氧化标志物如 4-羟基-2-壬烯醛（4-HNE）和 4-羟基-2-己烯醛（4-HHE）的水平。DHA 或姜黄素可拮抗这些作用，而姜黄素和 DHA 的组合对 DHA 和 4-HNE 具有增强作用。姜黄素和 DHA 的组合还能有效抵抗 TBI 后减少的可塑性标志物脑源性神经营养因子及其受体 p-trkB 和学习能力。
姜黄素补充了 DHA 对 TBI 病理的作用，这种特性似乎是一种可行的策略，可以对抗 TBI 后神经元功能障碍，并补充康复干预措施以促进功能恢复。
