中华耳科学杂志2011，Vol.9Issue(1)：87-91,5.
依达拉奉对抗化学性缺氧诱导的HEI-OC1听细胞内质网应激性凋亡
Protection against CoCl2-induced endoplasmic reticulum stress and apoptosis in HEI-OC1 cells by edaravone
曹磊 1张世平 1胡亿文1
作者信息
- 1. 广州市红十字会医院耳鼻喉科,广州,510220
- 折叠
摘要
Abstract
Objective To study whether edaravone (EDA) can protect HEI-OC1 (House Ear Institute -organ of Corti 1) auditory cells (HEI-0C1 cells) against CoCl2-induced endoplasmic reticulum stress (ERS) and apoptosis. Methods HEI-0C1 cells were treated with CoCl2 as a model of hypoxic auditory cellular toxicity. EDA was added into the culture medium before CoCl2 treatment as a pretreatment. Cell viability was measured with cell counter kit (CCK-8). Intracellular malondialdehyde (MDA) level was detected by a commercial kit. The expressions of glucose regulating protein 78 (GRP78) and cleaved caspase-12 were evaluated by Western blot assay. Results Exposure of HEI-OC1 cells to CoCl2 at 100-400 (unol/L for 24 h decreased cell viability in a dose-dependent manner. Pre-treatment with 300 u,mol/L C0CI2 resulted in over-expressions of CRP78 and cleaved caspase-12, as well as an increase in intracellular MDA level in HEI-OC1 cells. Pretreatment of EDA at 10-40 u,mol/L inhibited CoCl2 treatment-induced cytotoxicity in a concentration-dependently manner. Pretreatment of 40 n-mol/L EDA suppressed 300 u,mol/L C0CI2 treatment caused-upregulations of GRP78 and cleaved caspase-12, as well as the increase in intracellular MDA level. Conclusion EDA can protect HEI-0C1 cells against CoCl2-induced injury, via anti-oxidation and anti-ERS -mediated apoptosis关键词
依达拉奉/化学性缺氧/内质网应激/氧化应激/凋亡/HEI-OC1听细胞Key words
Edaravone/ Chemical hypoxia/ Endoplasmic reticulum stress/ Oxidative stress/ Apoptosis/ Auditory cells分类
医药卫生引用本文复制引用
曹磊,张世平,胡亿文..依达拉奉对抗化学性缺氧诱导的HEI-OC1听细胞内质网应激性凋亡[J].中华耳科学杂志,2011,9(1):87-91,5.
