Background
Lidocaine is a commonly used local anesthetic, and low-dose lidocaine has neuroprotective effects on cerebral ischemia/reperfusion (CI/R) injury; the mechanism for this, however, is still unclear. The
Conclusions
The results indicate that lidocaine protects against cerebral injury induced by I/R in rats via the nuclear factor kappa-B (NF-κB) p65 and p38 mitogen-activated protein kinase (MAPK) signaling pathway, it provided a candidate for the treatment of CI/R-induced injury.
Methods
We constructed a rat (male Sprague-Dawley rats, 6-8 weeks old) model of CI/R injury induced by middle cerebral artery occlusion (MCAO). Histopathology, neuronal apoptosis, oxidative stress, and inflammatory response were evaluated using hematoxylin and eosin (HE) staining, Nissl staining, enzyme-linked immunosorbent assay (ELISA) and western blotting, respectively. In addition, brain water content, infarct volume, neurological deficit score each evaluated.
Results
The findings showed that lidocaine improved spatial learning and memory impairment, protected I/R-induced brain injury and attenuated neuronal death and apoptosis. Furthermore, lidocaine also regulated the levels of malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), IL-6, IL-10, iNOS, and IL-4.Notably, lidocaine markedly inhibited the expression of p65 and p38. Conclusions: The results indicate that lidocaine protects against cerebral injury induced by I/R in rats via the nuclear factor kappa-B (NF-κB) p65 and p38 mitogen-activated protein kinase (MAPK) signaling pathway, it provided a candidate for the treatment of CI/R-induced injury.