Long non-coding RNA MALAT1 in apoptosis and oxidative stress of human lens epithelial cells
10.3980/j.issn.1672-5123.2026.9.03
- VernacularTitle:长链非编码RNA MALAT1对人晶状体上皮细胞凋亡和氧化应激的作用
- Author:
Xiaoming DONG
1
;
Yuxuan LIU
1
;
Yifei WANG
1
;
Dong LI
1
;
Jinsong ZHANG
1
;
Jing WANG
1
Author Information
1. Aier Group Cataract and Intraocular Lens Research Institute, Shenyang 110000, Liaoning Province, China; Shenyang Aier Eye Precision Medical Research Institute,Shenyang 110000, Liaoning Province, China; Liaoning Aier Eye Hospital Co., Ltd.,Shenyang 110000, Liaoning Province, China; Yingkou Vocational & Technical College, Yingkou 115000, Liaoning Province, China
- Publication Type:Journal Article
- Keywords:
lens epithelial cells;
long non-coding RNA;
metastasis-associated lung adenocarcinoma transcript 1(MALAT1);
apoptosis;
oxidative stress
- From:
International Eye Science
2026;26(9):1517-1523
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To clarify the expression characteristics and regulatory role of the long non-coding RNA(lncRNA)metastasis-associated lung adenocarcinoma transcript 1(MALAT1)in oxidative stress and apoptosis of H2O2-induced human lens epithelial cell line HLE-B3.METHODS: HLE-B3 cells were divided into Control group and H2O2 group(cultured with 200 μmol/L H2O2 for 24 h). Levels of reactive oxygen species(ROS)and cell apoptosis rates were detected by flow cytometry. Activities of superoxide dismutase(SOD)and catalase(CAT)were measured using kits, MALAT1 expression was quantified by real-time quantitative PCR, and its cellular localization was determined by fluorescence in situ hybridization. After selecting the Si-MALAT1 sequence with the highest silencing efficiency, the groups were established as Control, H2O2, H2O2+Si-NC, and H2O2+Si-MALAT1. Immunofluorescence staining was employed to detect the apoptosis marker TUNEL and Nrf2 nuclear translocation. RESULTS:Compared with the Control group, the H2O2group exhibited significantly elevated ROS levels, markedly decreased SOD and CAT activities(both P<0.001), and a significantly increased apoptosis rate(P<0.01). MALAT1 expression was upregulated(P<0.01)and localized in the nucleus. After silencing MALAT1, H2O2-induced cell apoptosis was significantly inhibited(P<0.01).CONCLUSION: H2O2-induced oxidative stress can increase the expression of MALAT1, and silencing MALAT1 reduces oxidative stress damage and apoptosis, providing a potential target for preventing and treating cataracts.
