首页|雌激素对D-半乳糖诱导的HEI-OC1细胞氧化应激损伤的作用

雌激素对D-半乳糖诱导的HEI-OC1细胞氧化应激损伤的作用

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目的 探讨雌激素对D-半乳糖诱导耳蜗毛细胞氧化应激的影响及相关分子机制.方法 体外培养小鼠耳蜗毛细胞株 HEI-OC1(house ear institute-organ of Corti 1),分为空白对照组、D-半乳糖组(20 mg/mL)和雌激素+D-半乳糖组(20 mg/mL D-半乳糖+10 nmol/L β-雌二醇).CCK-8法检测各组HEI-OC1细胞增殖情况;利用DCFH-DA探针技术检测各组HEI-OC1细胞内的ROS含量;利用超氧化物歧化酶(SOD)试剂盒检测各组HEI-OC1细胞内氧化应激因子SOD含量;Western blot检测各组细胞核因子E2相关蛋白(Nrf2)、血红素加氧酶(HO-1)的蛋白表达水平.结果 与空白对照组相比,D-半乳糖组细胞增殖活性减弱(P<0.01),ROS含量显著上升(P<0.01),SOD活力和Nrf2、HO-1蛋白表达水平显著下降(P<0.01).与D-半乳糖组相比,雌激素+D-半乳糖组细胞增殖活性增加(P<0.01),ROS水平显著下降(P<0.01),同时,SOD活力和Nrf2、HO-1蛋白表达水平显著上升(P<0.01).结论 雌激素能够通过Nrf2/HO-1通路缓解D-半乳糖诱导的HEI-OC1细胞氧化应激所造成的损伤.
Effect of estrogen on D-galactose-induced oxidative stress injury of HEI-OC1 cells
Objective To investigate the effect of estrogen on D-galactose-induced oxidative stress in cochlear hair cells.Methods The mouse cochlear hair cell line HEI-OC1 was cultured in vitro,and then divided into blank control group,D-galactose group(20 mg/mL)and estrogen+D-galactose group(20 mg/mL D-galactose+10 nmol/L β-estradiol).CCK-8 was used to detect the proliferation of HEI-OC1 cells in each group.DCFH-DA probe technology was used to detect ROS content in HEI-OC1 cells in each group.Superoxide dismutase(SOD)kit was used to detect the content of SOD in HEI-OC1 cells in each group.Western blot was used to detect the protein expression levels of nuclear factor E2-related protein(Nrf2)and heme oxygenase(HO-1)in each group.Results Compared with blank control group,the cell proliferation activity was decreased in D-galactose group(P<0.01),ROS content was increased(P<0.01),and SOD activity and Nrf2 and HO-1 protein expression levels were significantly decreased(P<0.01).Compared with D-galactose group,the cell proliferation activity was increased in estrogen+D-galactose group(P<0.01),ROS level was decreased(P<0.01),and SOD activity and Nrf2 and HO-1 protein expression levels were significantly increased(P<0.01).Conclusion Estrogen can alleviate the damage caused by D-galactose-induced oxidative stress in HEI-OC1 cells through Nrf2/HO-1 pathway.

estrogenHEI-OC1 cellsoxidative stressreactive oxygen speciesNrf2/HO-1 signaling pathway

张李娜、桑亚茹、王光辉、徐贝贝、韩跃峰

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蚌埠医科大学第一附属医院耳鼻喉头颈外科,蚌埠 233000

雌激素 HEI-OC1细胞 氧化应激 活性氧 核因子E2因子相关因子2/血红素加氧酶1通路

2024

山西医科大学学报
山西医科大学

山西医科大学学报

CSTPCD
影响因子:0.931
ISSN:1007-6611
年,卷(期):2024.55(4)
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