Department of Pharmacology, Toxicology, and Therapeutics, University of Kansas Medical Center, 3901 Rainbow Blvd., Kansas City, KS 66160, USA.
Prostaglandins Leukot Essent Fatty Acids. 2013 Aug;89(2-3):97-105. doi: 10.1016/j.plefa.2013.05.004. Epub 2013 Jun 21.
The effects of dietary modulation of brain DHA content on outcomes after TBI were examined in a juvenile rat model. Long-Evans rats with normal or diet-induced decreases in brain DHA were subjected to a controlled cortical impact or sham surgery on postnatal day 17. Rats with the greatest decreases in brain DHA had the poorest sensorimotor outcomes after TBI. Ccl2, Gfap, and Mmp 9 mRNA levels, and MMP-2 and -9 enzymatic activities were increased after TBI regardless of brain DHA level. Lesion volume was not affected by brain DHA level. In contrast, TBI-induced Timp1 expression was lower in rats on the Deficient diet and correlated with brain DHA level. These data suggest that decreased brain DHA content contributes to poorer sensorimotor outcomes after TBI through a mechanism involving modulation of Timp1 expression.
本研究旨在探讨饮食调控大脑 DHA 含量对 TBI 后结局的影响,采用幼年大鼠模型进行研究。对正常饮食或饮食诱导 DHA 降低的长爪沙鼠于生后第 17 天进行皮质撞击或假手术。与 TBI 后大脑 DHA 降低程度最显著的大鼠相比,大脑 DHA 降低程度最显著的大鼠的感觉运动功能结局最差。无论大脑 DHA 水平如何,TBI 后 Ccl2、Gfap 和 Mmp9mRNA 水平以及 MMP-2 和 -9 的酶活性均增加。脑损伤体积不受大脑 DHA 水平的影响。相反,在 DHA 缺乏饮食组大鼠中,TBI 诱导的 TIMP1 表达降低,且与大脑 DHA 水平相关。这些数据表明,大脑 DHA 含量降低可能通过调节 TIMP1 表达而导致 TBI 后感觉运动功能结局较差。