Role of ERK signaling pathway in dexmedetomidine against mouse neuroblastoma N2a cell injury induced by oxidative stress
- VernacularTitle:ERK信号通路在右美托咪定减轻小鼠神经母细胞瘤细胞氧化应激损伤中的作用
- Author:
Wenjing ZHAO
1
;
Zhuqing RAO
;
Cunming LIU
Author Information
- Keywords: Dexmedetomidine; Neuroblastoma; Oxidative stress injury; ERK signaling pathway
- From: The Journal of Clinical Anesthesiology 2018;34(5):493-496
- CountryChina
- Language:Chinese
- Abstract: Objective To investigate the role and underlying mechanism of dexmedetomidine in protecting mouse neuroblastoma N2a cells against oxidative stress injury,and to discuss the effect of ERK signaling pathway.Methods Na2 cell oxidative stress injury model was established by H2O2 treatment.Cells were divided into 5 groups:control group (group C),H2O2group (group H), dexmedetomidine group (group D),H2O2+dexmedetomidine group (group HD),H2O2+dexme-detomidine+ERK inhibitor group (group HDP).Group H,group HD and group HDP were given 200 μmol/L H2O2with or without 100 ng/ml dexmedetomidine and 20 μmol/L ERK inhibitor PD98059,group D was treated with dexmedetomidine at the corresponding point,group C was treated with equal normal saline,After 1,4 hours of H2O2stimulation,cell survival,morphology changes,SOD production and ERK intracellular signaling pathway were compared between groups. Results Compared to group C,N2a cells in the group H demonstrated significantly ruduced cell sur-vival,much worse cell morphology and less SOD production (P<0.05).Compared to group H,N2a cells in group HD demonstrated significantly increased cell survival,much better preserved cell mor-phology,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 (P<0.05).No significant changes were found in cell survival,morphology changes,SOD pro-duction and ERK intracellular signaling pathway between the groups C and D.Conclusion Dexme-detomidine protected mouse neuroblastoma N2a cells against oxidative stress injury by regulating ERK activation and SOD production.
