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AIM: To investigate the role of c-Jun N-terminal protein kinase 1 and 2 (JNK1/2) and the main signal pathway forits activation in hydrogen peroxide (H2O2) induced apoptotic-like cortical cell death. METHODS: Using the modelof oxidative stress induced by H2O2, the expression and diphosphorylation of JNK1/2 was examined by immunoblottinganalysis, and neuronal apoptotic like cell death was determined by 4’,6-diamidino-2-phenylindole (DAPI) staining.RESULTS: The elevation in diphosphorylation level of JNK1/2 (4.40-/5.61-fold vs sham control) was associatedwith the concentration of H2O2 (0-100 mol/L) and the development of apoptotic-like cell death (11.04 %-81.01 %).There was no alteration of JNK1/2 protein expression following H2O2 treatment and recovery at different timepoints. Administration with JNK1/2 antisense oligonucleotides not only significantly decreased JNK1/2 proteinexpression and activation level, but also significantly reduced cortical cell death induced by H2O2 exposure.Furthermore, both JNK1/2 diphosphorylation and apoptotic-like cell death were largely prevented by pretreatmentwith (5S,10R)-()-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine hydrogen maleate (MK-801)or omission of Ca2+ in incubation medium with ethylene glycol-bis(2-aminoethylether)-N,N,N’,N’-tetraacetic acid(EGTA). CONCLUSION: JNK1/2 is activated and participates in H2O2-induced apoptotic-like death in cultured ratcortical neurons mainly via N-methyl-D-aspartate (NMDA) receptor-mediated influx of extracellular Ca2+.
AIM: To investigate the role of c-Jun N-terminal protein kinase 1 and 2 (JNK1 / 2) and the main signal pathway for in activation in hydrogen peroxide (H2O2) induced apoptotic-like cortical cell death. METHODS: Using the model of oxidative stress induced by H2O2, the expression and diphosphorylation of JNK1 / 2 was examined by immunoblotting analysis, and neuronal apoptotic like cell death was determined by 4 ’, 6-diamidino-2-phenylindole (DAPI) staining .RESULTS: The elevation in diphosphorylation level of There was no alteration of H2O2 (0-100 mol / L) and the development of apoptotic-like cell death (11.04% -81.01%) JNK1 / 2 (4.40- / 5.61-fold vs sham control) was associated with the concentration of H2O2 JNK1 / 2 protein expression following H2O2 treatment and recovery at different timepoints. Administration with JNK1 / 2 antisense oligonucleotides not only significantly decreased JNK1 / 2 proteinexpression and activation level, but also significantly reduced cortical cell death induced by H2O2 exposure. Fu rthermore, both JNK1 / 2 diphosphorylation and apoptotic-like cell death were prevented by pre treatment with (5S, 10R) - () - 5-methyl- 10,11-dihydro- 5H-dibenzo [a, d] cyclohepten-5,10 -imine hydrogen maleate (MK-801) or omission of Ca2 + in incubation medium with ethylene glycol-bis (2-aminoethylether) -N, N, N’N’-tetraacetic acid (EGTA) and participates in H2O2-induced apoptotic-like death in cultured rat cortical neurons mainly via N-methyl-D-aspartate (NMDA) receptor-mediated influx of extracellular Ca2 +.