Abstract
Spinal cord injury (SCI) often results in abnormal sensory and motor functions. Current interventions for SCI in the clinical setting are not effective partly due to the complexity concerning its pathophysiological mechanism. In the wake of SCI, considerable inflammatory cells assemble around the injured area that induces a series of inflammatory reactions and aggravates tissue lesions, thereby affecting the recovery of the damaged nerve tissue. Therefore, the inhibition of inflammatory responses can improve the repair of the injured spinal cord tissue. Safflower Yellow (SY) is the main active ingredient of Carthamus tinctorius. SY has anti-inflammatory effect, as it can inhibit IκBα phosphorylation to impede the NF-κB signaling pathway and p53 nuclear translocation. Besides, SY can limit the release of pro-inflammatory factors, which in turn may alleviate secondary SCI and prevent further complications. In this report, we analyze the pathophysiological mechanism of SCI, the role of inflammatory responses, and how SY interferes with the HMGB1-TLR-4-NF-κB signaling pathway to attenuate inflammatory responses in SCI.
Highlights
Spinal cord injury (SCI) is a serious central nervous system injury (Ahuja et al, 2017; Hodgetts and Harvey, 2017)
Microglia appears to be strongly related to chronic neuroinflammation after SCI, and microglial cells expressing TNF-α may transform the polarization of astrocytes to neurotoxic phenotypes (Yoshizaki et al, 2021)
Safflower Yellow (SY) may mitigate the release of pro-inflammatory factors, TNF-α, IL-1β, and interleukin 6 (IL-6)
Summary
Spinal cord injury (SCI) is a serious central nervous system injury (Ahuja et al, 2017; Hodgetts and Harvey, 2017). Primary SCI is usually a mechanical damage that causes the destruction of the blood spinal cord barrier and induces local inflammatory responses (Stahel et al, 2012). SCI can give rise to a comprehensive inflammatory cascade response induced by the activation of innate immune cells (microglia and astrocyte), leukocytes (neutrophil and macrophage), and neuronal cell death.
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