The NFATC2/Nrf2 cascade regulates spinal cord ischemia-reperfusion injury by controlling inflammation, apoptosis and oxidative stress

Spinal cord ischemia/reperfusion (IR) injury (SCII) can cause major autonomic, sensory, and motor damage and loss. The upregulation of Nrf2, a primary orchestrator of the oxidative stress response, has beneficial effects in SCII. Here, we aimed to uncover a SCII-related transcription factor that is able to elevate Nrf2 expression. Rat PC12 cells were subjected to treatment with oxygen-glucose deprivation/reoxygenation (OGD/R) to induce an in vitro neuronal IR injury model. Our study demonstrates that the NFATC2/Nrf2 cascade has a regulatory capacity in inflammation, apoptosis and oxidative stress after SCII.

• 1
  Nrf2 and NFATC2 levels were reduced in PC12 cells after OGD/R treatment.
• 2
  Mechanistically, NFATC2 could activate Nrf2 transcription and promote its expression.
• 3
  Nrf2 reduction exerted a counteracting impact on NFATC2's anti-inflammation, anti-apoptosis and anti-oxidative stress functions in PC12 cells under OGD/R conditions.