Apolipoprotein E Deficiency Exacerbates Spinal Cord Injury in Mice: Inflammatory Response and Oxidative Stress Mediated by NF-κB Signaling Pathway

Spinal cord injury (SCI) leads to complex pathological processes including inflammation and oxidative stress, which affect functional recovery. Apolipoprotein E (APOE) is known to induce neuronal repair, but its exact role in mediating inflammatory and oxidative stress pathways after SCI is unclear. This study investigates how APOE deficiency affects inflammatory response and oxidative stress in the acute stage of SCI using Apoe−/− mice. The results show that Apoe−/− mice had impaired functional recovery, increased inflammation, and oxidative stress after SCI. The study also found that the absence of Apoe increased inflammation and oxidative stress through the activation of NF-κB. Inhibiting NF-κB alleviated these changes, indicating that NF-κB plays a critical role in Apoe-deficiency dependent inflammation and oxidative stress, which are detrimental to recovery after SCI.

• 1
  Apoe−/− mice showed retarded functional recovery and a larger lesion size compared to wild-type mice after SCI, indicating that Apoe deficiency worsens the outcomes after SCI.
• 2
  Deficiency of Apoe induced an exaggerated inflammatory response by increasing the expression of interleukin-6 (IL-6) and interleukin-1β (IL-1β), and increased oxidative stress by reducing the expression of Nrf2 and HO-1.
• 3
  The absence of Apoe increased inflammation and oxidative stress through activation of NF-κB after SCI, and inhibiting NF-κB alleviated these changes, highlighting the critical role of NF-κB in Apoe-deficiency dependent inflammation and oxidative stress.