Expression of APE/Ref-1 in cultured rat spiral ganglion cells after oxidative damage induced by H<sub>2</sub>O<sub>2</sub>

姜振东; 张学渊; 魏运军; 袁伟; 卓贤露

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Expression of APE/Ref-1 in cultured rat spiral ganglion cells after oxidative damage induced by H₂O₂

更新时间：2026-01-09

- Expression of APE/Ref-1 in cultured rat spiral ganglion cells after oxidative damage induced by H₂O₂
- Journal of Army Medical University Vol. 29, Issue 5, Pages: 435-438(2007)
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  CLC： R322.923;R329.28;R341
- Published：2007
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姜振东,张学渊,魏运军,袁伟,卓贤露.APE/Ref1在H2O2诱导耳蜗螺旋神经节细胞氧化损伤过程中的表达[J].陆军军医大学学报(原第三军医大学学报),2007,29(05):435-438.

　JIANG Zhen-dong,ZHANG Xue-yuan,WEI Yun-jun,YUAN Wei,ZHUO Xian-lu.Expression of APE/Ref-1 in cultured rat spiral ganglion cells after oxidative damage induced by H2O2[J].J Amry Med Univ (J Third Mil Med Univ),2007,29(05):435-438.
姜振东,张学渊,魏运军,袁伟,卓贤露.APE/Ref1在H2O2诱导耳蜗螺旋神经节细胞氧化损伤过程中的表达[J].陆军军医大学学报(原第三军医大学学报),2007,29(05):435-438. DOI：

　JIANG Zhen-dong,ZHANG Xue-yuan,WEI Yun-jun,YUAN Wei,ZHUO Xian-lu.Expression of APE/Ref-1 in cultured rat spiral ganglion cells after oxidative damage induced by H2O2[J].J Amry Med Univ (J Third Mil Med Univ),2007,29(05):435-438. DOI：

摘要

目的研究氧化还原因子-1（apurinic/apyrimidimic endonuclase/redox factor 1

APE/Ref-1）在过氧化氢(H

)诱导耳蜗螺旋神经节细胞(spiral ganglion cells

SGCs)氧化损伤过程中的表达。方法原代培养离体大鼠SGCs，采用免疫荧光和Western blot方法检测APE/Ref-1在H

诱导SGCs 氧化损伤过程中的表达。台盼蓝染色法计算SGCs氧化损伤过程中的死亡率。结果 APE/Ref-1在体外正常培养SGCs细胞质和细胞核均有表达，细胞核较强。H

浓度≥60 μmol/L 时， SGCs死亡率显著升高，APE/Ref-1在细胞核表达明显减弱，与对照组相比差异具有统计学意义(P 0.05)。结论 APE/Ref-1在氧化环境下SGCs细胞核表达减少，细胞死亡率升高，提示氧化环境下细胞活性降低可能与APE/Ref-1表达减少有关。

Abstract

Objective To investigate the expression of apurinic/apyrimidimic endonuclase/redox factor 1 (APE/Ref-1) in primary cultured spiral ganglion cells (SGCs) after oxidative damage induced by H

exposure. Methods Rat SGCs were isolated and primarily cultured

and then exposed to H

at 30

100

300 μg/L for 24 h to induce oxidative damage. Immunofluorescence and immunoblotting were used to examine the expression of APE/Ref-1 in cultured SGC. The percent o

f cell death 24 h after exposure to H

was measured by trypan blue exclusion. Results APE/Ref-1 was highly expressed in primary cultured SGCs. APE/Ref-1 expression was significantly down-regulated and the percent of cell death was up-regulated at a dose of H

≥ 60 μmol/L. Conclusion The significant increase of cell death after oxidative stress may be related to reduction of APE/Ref-1 expression.

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Expression of APE/Ref-1 in cultured rat spiral ganglion cells after oxidative damage induced by H2O2

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摘要

Abstract

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references

Expression of APE/Ref-1 in cultured rat spiral ganglion cells after oxidative damage induced by H₂O₂