Abstract
Purpose: To investigate the neuroprotective effect of lidocaine in Neuro2A cells
 Methods: Differentiated N2a cells were used in this study. Cell viability and neuroprotection were assessed using dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and trypan blue assays, while Bax/Bcl-2 expression was assayed by western blotting. Mitochondrial membrane potential, reactive oxygen species and calcium levels were measured using flow cytometry.
 Results: Lidocaine protected differentiated N2a cells against cadmium-induced toxicity, and also attenuated cadmium toxicity-induced changes in mitochondrial membrane potential (MMP), reactive oxygen species (ROS) and calcium (Ca2+) levels. Furthermore, Bax/Bcl-2 ratio, which was disrupted by cadmium, and cadmium-induced apoptosis, were reversed by lidocaine.
 Conclusion: Lidocaine protects differentiated N2a cells against cadmium-induced toxicity by reversing apoptosis. Thus, lidocaine is a potential neuroprotective agent.
Highlights
The indispensable role of anesthetics in conferring neuroprotection has been greatly emphasized during post-operative procedures [1]
Neuroprotection can be achieved by limiting inflammatory damage from microglia and delaying cell death in neurons [2,3]
Inflammatory damage evoked during operative procedures causes the release of pro-inflammatory cytokines (TNF-α, IL-6 and IL-1β) from microglia
Summary
The indispensable role of anesthetics in conferring neuroprotection has been greatly emphasized during post-operative procedures [1]. Inflammatory damage evoked during operative procedures causes the release of pro-inflammatory cytokines (TNF-α, IL-6 and IL-1β) from microglia. These inflammatory cytokines act on neurons in their vicinity and direct their death. The inflammatory damage causes the release of ROS, thereby generating oxidative stress during which various inflammatory pathways (e.g. NF-kB and p38) are switched on in tremendously activated microglia [4,5]. These inflammatory events are detrimental to healthy neurons
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