Fromm Lisa, Heath Deanne L, Vink Robert, Nimmo Alan J
Department of Pathology, University of Adelaide, Adelaide, SA, Australia.
J Am Coll Nutr. 2004 Oct;23(5):529S-533S. doi: 10.1080/07315724.2004.10719396.
Magnesium (Mg) declines after traumatic brain injury (TBI), a decline believed associated with ensuing neuronal cell death and subsequent functional impairment. While Mg's effects on motor and cognitive deficits following TBI have been well studied, few studies have addressed post-traumatic depression as an outcome parameter, despite its being a major clinical problem with an incidence of between 6 and 77%. We investigated the incidence of post-traumatic depression/anxiety in an animal model of diffuse TBI, and explored the use of magnesium sulfate (MgSO(4)) as an interventional treatment.
Diffuse TBI was induced in 32 anesthetized, adult, male Sprague-Dawley rats, using the 2 m impact-acceleration model of injury. At 30 min after injury, half of the rats received 250 micromol/kg i.v. MgSO(4); the other half served as non-treated controls. Before and for 6 weeks after injury, the open-field, spontaneous activity test was used to determine post-traumatic depression/anxiety relative to pre-injury. In this test, animals are placed in a 1-meter square box with 100 squares marked on the base. The number of squares entered in a 5-min period is recorded. Incidence of post-traumatic depression/anxiety was defined as the number of animals demonstrating a reduction in spontaneous activity to less than 100 squares in 5 min. Prior to injury, rats typically entered a mean of 201 +/- 12 (SEM) squares over a 5 min observation period.
At 1 week after injury, non-treated animals had a mean core of 62 +/- 13. The incidence of post-traumatic depression/anxiety in these animals was 61%, which is similar to that observed clinically. In contrast, animals treated with MgSO(4) had a mean activity score of 144 +/- 23 at 1 week after TBI and an incidence of depression/anxiety of less than 30%. The significant difference between groups persisted for the entire 6-week observation period.
The improvement in post-traumatic depression/anxiety conferred by Mg adds further weight to available evidence of Mg's benefit as a neuroprotective agent after TBI.
创伤性脑损伤（TBI）后镁（Mg）水平会下降，这种下降被认为与随后的神经元细胞死亡及功能障碍有关。虽然Mg对TBI后运动和认知缺陷的影响已得到充分研究，但很少有研究将创伤后抑郁作为一个结果参数进行探讨，尽管它是一个主要的临床问题，发病率在6%至77%之间。我们在弥漫性TBI动物模型中研究了创伤后抑郁/焦虑的发生率，并探索了使用硫酸镁（MgSO₄）作为干预治疗手段。
采用2 m撞击-加速损伤模型，在32只麻醉的成年雄性Sprague-Dawley大鼠中诱导弥漫性TBI。损伤后30分钟，一半大鼠静脉注射250 μmol/kg MgSO₄；另一半作为未治疗对照。在损伤前及损伤后6周，使用旷场自发活动试验来确定相对于损伤前的创伤后抑郁/焦虑情况。在该试验中，将动物置于一个底面标有100个方格的1平方米正方形盒子中。记录5分钟内进入的方格数量。创伤后抑郁/焦虑的发生率定义为在5分钟内自发活动减少至少于100个方格的动物数量。在损伤前，大鼠在5分钟观察期内平均进入201±12（SEM）个方格。
损伤后1周，未治疗动物的平均方格数为62±13。这些动物中创伤后抑郁/焦虑的发生率为61%，与临床观察到的情况相似。相比之下，用MgSO₄治疗的动物在TBI后1周的平均活动评分为144±23，抑郁/焦虑发生率低于30%。两组之间的显著差异在整个6周观察期内持续存在。
Mg对创伤后抑郁/焦虑的改善作用进一步证明了Mg作为TBI后神经保护剂的益处。
