Journal of neurochemistry
-
Journal of neurochemistry · Apr 2014
Neuroprotective role of hydralazine in rat spinal cord injury-attenuation of acrolein-mediated damage.
Acrolein, an α,β-unsaturated aldehyde and a reactive product of lipid peroxidation, has been suggested as a key factor in neural post-traumatic secondary injury in spinal cord injury (SCI), mainly based on in vitro and ex vivo evidence. Here, we demonstrate an increase of acrolein up to 300%; the elevation lasted at least 2 weeks in a rat SCI model. More importantly, hydralazine, a known acrolein scavenger can provide neuroprotection when applied systemically. ⋯ Finally, the role of acrolein in SCI was further validated by the fact that acrolein injection into the spinal cord caused significant SCI-like tissue damage and motor deficits. Taken together, available evidence strongly suggests a critical causal role of acrolein in the pathogenesis of spinal cord trauma. Since acrolein has been linked to a variety of illness and conditions, we believe that acrolein-scavenging measures have the potential to be expanded significantly ensuring a broad impact on human health.
-
Journal of neurochemistry · Apr 2014
Vascular endothelial growth factor signaling in injured nerves underlies peripheral sensitization in neuropathic pain.
Chronic neuroinflammation may be a critical component of intractable inflammatory diseases, including neuropathic pain. Because angiogenesis as a result of vascular endothelial growth factor (VEGF) signaling plays a pivotal role in inflammation, we focused on the mechanisms of VEGF-regulated neuropathic pain in mice. The mRNA and protein expression of VEGFA were up-regulated in the injured sciatic nerve after partial sciatic nerve ligation (PSL). ⋯ VEGFA up-regulation and pathological angiogenesis were observed in the injured nerves in mice. Pharmacological inhibition of VEGF signaling suppressed neuropathic pain behaviors. Therefore, VEGFA-related components may underlie peripheral neuroinflammation leading to neuropathic pain.