Lidocaine mediates the progression of cerebral ischemia/yyyreperfusion injury in rats via inhibiting the activation of NF-κB p65 and p38 MAPK

Background: Lidocaine is a commonly used local anesthetic, and low-dose lidocaine has neuroprotective effects on cerebral ischetnia/reperfusion (CI/R) injury; the mechanism for this, however, is still unclear. The aim of this study was to investigate the role and the possible mechanisms of lidocaine on CI/R injury in rats. 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 (LIE) 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.NTotably, 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-kappa B) p65 and p38 mitogen-activated protein kinase (MAPK) signaling pathway, it provided a candidate for the treatment of CUR-induced injury.