Traumatic central nervous system injury can cause imbalance in intestinal microenvironmental homeostasis by disrupting intestinal barrier function, while the disturbed intestinal microenvironment can react on the central nervous system and aggravate the secondary injury of it. A large number of studies suggest that the intestinal barrier plays an important role in the pathophysiological process of traumatic central nervous system injury and can be an important target for the action of central nervous system injury. This paper reviews the structural and functional changes of intestinal microbial, chemical, mechanical and immune barriers after traumatic central nervous system injury and their bidirectional interaction with the central nervous system, summarizes the possible mechanisms leading to the disruption of intestinal barrier, including malnutrition, ischemia-reperfusion injury, inflammatory response and the release of neurotransmitters and hormones, to provide theoretical basis and new ideas for the development of research on the intestinal microenvironment after traumatic central nervous injury.

创伤性中枢神经系统损伤可通过破坏肠道屏障功能进而引起肠道微环境稳态失衡，而紊乱的肠道微环境可反作用于中枢，加重中枢神经系统继发性损伤。大量研究提示，肠道屏障在创伤性中枢神经损伤的病理生理过程中起重要作用，可作为中枢神经损伤的重要作用靶点。本文综述了创伤性中枢神经系统损伤后肠道微生物、化学、机械和免疫屏障结构和功能的变化及其与中枢的双向作用，并总结了致使肠屏障破坏的可能机制，包括营养不良、缺血再灌注损伤、炎性反应及神经递质和激素释放等，为创伤性中枢神经损伤后肠道微环境的研究开展提供一定的理论依据和新思路。