HSP70在化学性缺氧诱导毛细胞损伤中的作用

目的：探讨热休克蛋白70（heat shock protein 70,HSP70）在氯化钴（cobalt chloride,CoCl2）诱导听细胞损伤中的作用。方法：应用CoCl2处理HEI-OC1听细胞,建立化学性缺氧诱导耳蜗外毛细胞损伤的体外模型。细胞计数试剂盒-8（cell count kit 8,CCK-8）比色法检测细胞存活率,免疫印迹法（Western blot）检测HSP70的蛋白表达。结果：在150-750μmol/L浓度范围内,不同浓度的CoCl2处理听细胞24 h可引起明显的细胞毒性,使细胞存活率呈剂量依赖性地降低。300μmol/L CoCl2作用听细胞30-240 min可时间依赖性地上调HSP70的蛋白表达。HSP70抑制剂槲皮素（quercetin,Quer）可在蛋白水平下调CoCl2引起的听细胞内HSP70表达增加。Quer通过抑制HSP70的表达可加重CoCl2诱导的听细胞缺氧性损伤。结论：适应性HSP70表达增加可保护听细胞对抗缺氧诱导的损伤。

Roles of heat shock protein 70 in the cellular injury induced by chemical hypoxia in auditory cells

Objective： To explore the roles of heat shock protein 70（HSP70） in the cellular injury induced by chemical hypoxia in auditory cells.Methods： HEI-OC1 auditory cells were treated with cobalt chloride（CoCl2） to set up a chemical hypoxia-induced cochlear outer hair cells injury model.Cell viability was detected with cell counter kit 8（CCK-8）.The expression of HSP70 was evaluated by Western blot assay.Results： At concentrations of 150 to 750 μmol/L,treatment with CoCl2 for 24 h induced significant cytotoxicity in HEI-OC1 auditory cells.Treatment with 300 μmol/L CoCl2 from 30 to 240 min increased time-dependently the expression of HSP70.An inhibitor of HSP70,quercetin（Quer）,down-regulated in protein level the over-expression induced by CoCl2 treatment.By inhibiting HSP70 expression,Quer aggravated the cellular injury induced by CoCl2.Conclusion： Adaptive over-expression of HSP70 can protect auditory cells against the cellular injury induced by CoCl2.