依托咪酯和咪达唑仑对小鼠海马脑片细胞外信号调节激酶ERK1/2磷酸化水平的影响

目的观察依托咪酯和咪达唑仑对小鼠海马脑片细胞外信号调节激酶ERK1/2磷酸化水平的影响。方法BALB/C小鼠,雌雄不拘,取其海马制成厚450μm脑片,分别应用10-9~10-4mol/L依托咪酯和咪达唑仑在36℃恒温条件下孵育1 h。应用SDS-PAGE和Western blot等技术,用Gel Doc凝胶成像系统,半定量检测小鼠海马内p-ERK1/2的磷酸化水平。结果与对照组比较,在本研究应用的浓度范围内,咪达唑仑浓度的增加对ERK1/2磷酸化抑制程度无明显影响;在本研究所应用的浓度范围内,依托咪酯浓度的增加对ERK1磷酸化抑制程度无明显影响。随着依托咪酯浓度的增加,对ERK2磷酸化的抑制程度逐渐增加。结论依托咪酯和咪达唑仑可抑制小鼠海马脑片细胞外信号调节激酶ERK1/2磷酸化水平。在本研究应用的浓度范围内,随浓度的增加,依托咪酯对ERK2磷酸化水平的抑制程度逐渐增加。

Effects of Etomidate and Midazolam on Extracellular Signal-regulated Kinase1/2 Phosphorylation in Mice Hippocampal Slices

Objective To investigate the effects of etomidate and midazolam on extracellular signal-regulated kinase1/2 phosphorylation in mice hippocampus slices.Methods BALB/C mice weighting 18～22 g were decapitated and the hippocampus were dissected.Hippocampal slices were prepared with MacⅡwain tissue chopper.Hippocampal slices were incubated at 36 ℃ during the whole experiment.The slices were incubated with 10^-9～10^-4mol/L etomidate and midazolam respectively for 1h during the experiment.Phosphorylation of ERK1/2 was examined in hippocampus slices by immunoblotting with both phosphor-p44/42 Map kinase and p44/42 Map kinase antibodies.Experiments were performed in the absence(control) or presence of various concentrations of etomidate and midazolam.Results Clinically relevant concentrations of etomidate and midazolam decrease phosphorylation of ERK1/2.The decrease was concentration-dependent.Conclusion Etomidate and midazolam markedly decrease phosphorylation of ERK1/2 in mice hippocampal slices.