Spinal cord injury (SCI) is a type of central nervous system trauma that can lead to severe nerve injury. Inflammatory reaction after injury is an important pathological process leading to secondary injury. Long-term stimulation of inflammation can further deteriorate the microenvironment of the injured site, leading to the deterioration of neural function. Understanding the signaling pathways that regulate responses after SCI, especially inflammatory responses, is critical for the development of new therapeutic targets and approaches. Nuclear transfer factor-κB (NF-κB) has long been recognized as a key factor in regulating inflammatory responses. The NF-κB pathway is closely related to the pathological process of SCI. Inhibition of this pathway can improve the inflammatory microenvironment and promote the recovery of neural function after SCI. Therefore, the NF-κB pathway may be a potential therapeutic target for SCI. This article reviews the mechanism of inflammatory response after SCI and the characteristics of NF-κB pathway, emphasizing the effect of inhibiting NF-κB on the inflammatory response of SCI to provide a theoretical basis for the biological treatment of SCI.
Keywords: Apoptosis; Inflammation; Nuclear transfer factor-κB (NF-κB); Spinal cord injury (SCI); Targeted therapy.
© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.