[1]景瑞花,乔鑫利,薛菲.白内障氧化应激损伤诱导晶状体上皮细胞铁死亡[J].眼科新进展,2023,43(4):274-278.[doi:10.13389/j.cnki.rao.2023.0056]
 JING Ruihua,QIAO Xinli,XUE Fei.Ferroptosis of lens epithelial cells induced by oxidative stress injury of cataract patients[J].Recent Advances in Ophthalmology,2023,43(4):274-278.[doi:10.13389/j.cnki.rao.2023.0056]
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白内障氧化应激损伤诱导晶状体上皮细胞铁死亡/HTML
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《眼科新进展》[ISSN:1003-5141/CN:41-1105/R]

卷:
43卷
期数:
2023年4期
页码:
274-278
栏目:
实验研究
出版日期:
2023-04-05

文章信息/Info

Title:
Ferroptosis of lens epithelial cells induced by oxidative stress injury of cataract patients
作者:
景瑞花乔鑫利薛菲
710000 陕西省西安市,西安交通大学第二附属医院
Author(s):
JING RuihuaQIAO XinliXUE Fei
The Second Affiliated Hospital of Xi’an Jiaotong University,Xi’an 710000,Shaanxi Province,China
关键词:
晶状体上皮细胞氧化应激铁死亡紫外线
Keywords:
lens epithelial cells oxidative stress ferroptosis ultraviolet
分类号:
R776.1
DOI:
10.13389/j.cnki.rao.2023.0056
文献标志码:
A
摘要:
目的 本研究拟在白内障细胞模型中验证氧化应激损伤是否可诱导晶状体上皮细胞铁死亡。
方法 分别采用H2O2和紫外线B(UVB)模拟白内障氧化应激损伤模型并进行体外细胞实验。采用流式细胞术分别对H2O2组(0 h、12 h、24 h)和空白对照组、UVB组(UVB照射)进行晶状体上皮细胞死亡的检测,空白对照组不做任何处理。采用荧光探针染色观察和流式细胞术检测不同浓度(0 μmol·L-1、100 μmol·L-1、200 μmol·L-1和300 μmol·L-1)H2O2组和空白对照组、UVB组引起的晶状体上皮细胞C11/BODIPY染色阳性细胞率,表征细胞脂质过氧化水平。
结果 200 μmol·L-1 H2O2处理晶状体上皮细胞后,与0 h时相比,12 h时晶状体上皮细胞死亡率升高,但差异无统计学意义(P>0.05);24 h时晶状体上皮细胞死亡率显著升高,差异有统计学意义(P<0.01)。C11/BODIPY荧光探针染色结果显示,与空白对照组相比,50 μmol·L-1 H2O2组晶状体上皮细胞C11/BODIPY氧化态绿色荧光增强。H2O2可浓度梯度升高晶状体上皮细胞脂质过氧化水平,与0 μmol·L-1H2O2组相比,100 μmol·L-1 H2O2组、200 μmol·L-1 H2O2组晶状体上皮细胞C11/BODIPY荧光探针染色阳性细胞率均增加,但差异均无统计学意义(均为P>0.05);300 μmol·L-1 H2O2组晶状体上皮细胞C11/BODIPY荧光探针染色阳性细胞率显著增加,差异有统计学意义(P<0.05)。与空白对照组相比,UVB组晶状体上皮细胞死亡率增加,差异有统计学意义(P<0.05),但以细胞凋亡方式为主。与空白对照组相比,UVB组晶状体上皮细胞C11/BODIPY荧光探针染色阳性细胞率增加,差异有统计学意义(P<0.05)。
结论 H2O2和UVB均可直接诱导晶状体上皮细胞铁死亡和脂质过氧化水平升高,可能是白内障潜在发病机制。
Abstract:
Objective To verify whether oxidative stress injury could induce ferroptosis of lens epithelial cells (LECs) in the cataract cell model.
Methods Hydrogen peroxide (H2O2) and ultraviolet (UVB) were used to establish the cataract oxidative stress injury model and conduct the in vitro cell experiment. Flow cytometry was used to count the dead LECs after treatment in the H2O2 group (0 h, 12 h and 24 h), blank control group and UVB group (UVB irradiation). The cells in the blank control group received no treatment. The C11/BODIPY fluorescent probe staining and flow cytometry were adopted to detect the positive rate of LECs in the H2O2 group (0 μmol·L-1, 100 μmol·L-1, 200 μmol·L-1 and 300 μmol·L-1), blank control group and UVB group, representing the degree of lipid peroxidation level.
Results After the treatment of LECs with 200μmol·L-1 H2O2, compared with the 0h treatment sub-group, the death rate of LECs in the 12 h treatment sub-group increased, with no significant difference (P>0.05), and that in the 24h treatment sub-group increased significantly (P<0.01). C11/BODIPY fluorescent probe staining results showed that, compared with the blank control group, 50 μmol·L-1 H2O2 induced noticeable C11/BODIPY oxidation state fluorescence enhancement. H2O2 could increase the lipid peroxidation level of LECs in a concentration-dependent manner. Compared with the 0 μmol·L-1 H2O2 sub-group, the positive rate of LECs in the C11/BODIPY fluorescent probe staining increased in the 100 μmol·L-1 H2O2 sub-group and 200 μmol·L-1 H2O2 sub-group, with no significant difference (both P>0.05), and significantly increased in the 300 μmol·L-1 H2O2 sub-group (P<0.05). Compared with the blank control group, the death rate of LECs significantly increased (P<0.05), most in the way of apoptosis, and the positive rate of LECs in the C11/BODIPY fluorescent probe staining also significantly increased in the UVB group (P<0.05).
Conclusion Both H2O2 and UVB can directly induce the ferroptosis of LECs and aggravate the lipid peroxidation level, thus they may be the potential pathogenesis of cataracts.

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备注/Memo

备注/Memo:
国家自然科学基金(编号:82201163);陕西省自然科学基金青年基金(编号:2023-JC-QN-0861)
更新日期/Last Update: 2023-04-05