Ischemia reperfusion injury

see Cerebral ischemia-reperfusion injury.

sse Spinal cord ischemia reperfusion injury.

Previous studies have shown that Ischemia reperfusion injury (IRI) contributes to the injury process in the central nervous system (CNS), through the activation of the immune system 1) 2) 3) 4) 5).

1)
Gökce EC, et al. Neuroprotective effects of thymoquinone against spinal cord ischemia-reperfusion injury by attenuation of inflammation, oxidative stress, and apoptosis. J Neurosurg Spine. 2016;24(6):949–959. doi: 10.3171/2015.10.SPINE15612.
2)
Dimitrijevic OB, Stamatovic SM, Keep RF, Andjelkovic AV. Absence of the chemokine receptor CCR2 protects against cerebral ischemia/reperfusion injury in mice. Stroke. 2007;38(4):1345–1353. doi: 10.1161/01.STR.0000259709.16654.8f.
3)
Chen Y, et al. Overexpression of monocyte chemoattractant protein 1 in the brain exacerbates ischemic brain injury and is associated with recruitment of inflammatory cells. J Cereb Blood Flow Metab. 2003;23(6):748–755.
4)
Smith PD, et al. The evolution of chemokine release supports a bimodal mechanism of spinal cord ischemia and reperfusion injury. Circulation. 2012;126(11 Suppl 1):S110–S117.
5)
Strecker JK, Minnerup J, Gess B, Ringelstein EB, Schäbitz WR, Schilling M. Monocyte chemoattractant protein-1-deficiency impairs the expression of IL-6, IL-1β and G-CSF after transient focal ischemia in mice. PLoS One. 2011;6(10):e25863 doi: 10.1371/journal.pone.0025863.