School of Medical Sciences, University of Adelaide, Adelaide, South Australia, Australia.
Neurotherapeutics. 2010 Jan;7(1):74-80. doi: 10.1016/j.nurt.2009.10.018.
Although a number of secondary injury factors are known to contribute to the development of morphological injury and functional deficits following traumatic brain injury, accumulating evidence has suggested that neuropeptides, and in particular substance P, may play a critical role. Substance P is released early following acute injury to the CNS as part of a neurogenic inflammatory response. In so doing, it facilitates an increase in the permeability of the blood-brain barrier and the development of vasogenic edema. At the cellular level, substance P has been shown to directly result in neuronal cell death; functionally, substance P has been implicated in learning and memory, mood and anxiety, stress mechanisms, emotion-processing, migraine, emesis, pain, and seizures, all of which may be adversely affected after brain injury. Inhibition of post-traumatic substance P activity, either by preventing release or by antagonism of the neurokinin-1 receptor, has consistently resulted in a profound decrease in development of edema and marked improvements in functional outcome. This review summarizes the current evidence supporting a role for substance P in acute brain injury.
尽管已知许多继发性损伤因素会导致创伤性脑损伤后形态损伤和功能缺陷的发展，但越来越多的证据表明，神经肽，尤其是 P 物质，可能起着关键作用。P 物质在中枢神经系统急性损伤后作为神经源性炎症反应的一部分被早期释放。这样做可以促进血脑屏障通透性的增加和血管源性水肿的发展。在细胞水平上，已证明 P 物质直接导致神经元细胞死亡；在功能上，P 物质与学习和记忆、情绪和焦虑、应激机制、情绪处理、偏头痛、呕吐、疼痛和癫痫有关，这些在脑损伤后都可能受到不利影响。通过防止释放或拮抗神经激肽-1 受体来抑制创伤后 P 物质的活性，始终导致水肿的发展明显减少，并显著改善功能结果。这篇综述总结了支持 P 物质在急性脑损伤中起作用的现有证据。
