摘要
目的:观察过氧化氢(H2O2)对大鼠螺旋神经节细胞(SGCs)的作用,探讨氧自由基损伤SGCs的机制。方法:新生大鼠SGCs原代培养,取培养第4天细胞加入H2O2,浓度分别为0、100、200、500μmol/L,作用2、4、6 h,光镜下观察细胞形态改变,hochest33258及PI染色,计数受损伤细胞的百分比。结果:在H2O2的作用下,原代培养的SGCs随着H2O2浓度的增加以及作用时间的延长,受损伤的细胞数目呈增加趋势。同时,低浓度(100及200μmol/L)H2O2作用下,SGCs的损伤主要以凋亡表现为主,PI染色多为阴性;高浓度H2O2(500μmol/L)作用下的SGCs损伤以坏死为主。结论:H2O2可以引起SGCs凋亡,且作用有明显的剂量及时间依赖性。凋亡的发生可能和凋亡相关基因的启动有关,但仍需进一步实验证实。
Objective：To make clear the molecular pathways involved in hydrogen peroxide-induced spiral gan glion cells death. Method：The spiral ganglion cells of the newly born rats were primary cultured. Then the SGCs were exposed to hydrogen peroxide for different concentrations （0,100,200,500 μmol/L） and for different hours （2,4,6 h）. Cell nucleis were stained simultaneously with the DNA binding dyes Hoechst 33258 and propidium io dide. Result： At lower concentrations of hydrogen peroxide, apoptosis was the main reason for cell death. At higher concentrations of hydrogen peroxide, the cells died mainly by necrosis. Conclusion：The effects of hydrogen peroxide are dose and time dependency. Reactive oxygen species may play a role as an early molecule signal in the mechanisrn of SGCs death.
出处
《临床耳鼻咽喉头颈外科杂志》
CAS
CSCD
北大核心
2009年第5期222-224,共3页
Journal of Clinical Otorhinolaryngology Head And Neck Surgery
基金
国家自然科学基金资助项目(No:30471879)
高校青年教师奖
湖北省卫生厅科研基金资助项目(No:JXIBO56)
关键词
氧化应激
过氧化氢
凋亡
螺旋神经节
oxidative stress
hydrogen peroxide
apoptosis
spiral ganglion
