Role Of ERK Signaling Pathway In Dexmedetomidine Against Mouse Neuroblastoma N2a Cell Injury Induced By Oxidative Stress

Objective To investigate the role and underlying mechanism of dexmedetomidine in protecting mouse neuroblastoma N2 a cells against oxidative stress injury.Methods Na2 cell oxidative stress injury model was established by H2O2 treatment.Cells were divided into 8 groups: Control group(group C),H2O2 group(group H),dexmedetomidine group(group D),H2O2 + dexmedetomidine group(group HD),ERK inhibitor group(group PD),H2O2 + ERK inhibitor group(group HP),dexmedetomidine + ERK inhibitor group(group DP),H2O2 + dexmedetomidine + ERK inhibitor group(group HDP).After 1,4 hours of H2O2 stimulation,cell survival,morphology changes,SOD production and intracellular signaling pathway including p-ERK,apoptosis-related Bcl2 and Bax were compared between groups.Results Compared to group H,N2 a cells in the group HD demonstrated significantly increased cell survival,much better preserved cell morphology,higher levels of SOD and enhanced ERK activation(P<0.05);Compared to group HD,cells in the group HDP had markedly decreased cell survival,worse cell morphology and lower SOD level.No significant changes were found in the activation of Bcl-2 and Bax between the group H and HD.Conclusion Dexmedetomidine protected mouse neuroblastoma N2 a cells against oxidative stress injury by regulating ERK activation and SOD production,but not apoptosis-related Bcl-2 and Bax signaling pathway.