ReferenceID 1783
Diosmetin attenuates oxidative stress-induced damage to lens epithelial cells via the mitogen-activated protein kinase (MAPK) pathway
Bioengineered
Cataract is a global ophthalmic disease that blinds the eye, and oxidative stress is one of its primary causes. Apoptosis of lens epithelial cells (LECs) is considered the major cytological basis of many cataracts except
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Record Fields
Scalar fields from the final reference record.
- Reference Id
- 1783
- Evidence Id
- 18373
- Core Evidence Id
- 18373
- Source Reference Id
- 3561
- Herb2 Reference Id
- HBREF004358
- Subject Paper Key
- HBIN024184_35481411
- Pubmed Id
- 35481411
- Doi
- 10.1080/21655979.2022.2068755
- Paper Title
- Diosmetin attenuates oxidative stress-induced damage to lens epithelial cells via the mitogen-activated protein kinase (MAPK) pathway
- Paper Abstract
- Cataract is a global ophthalmic disease that blinds the eye, and oxidative stress is one of its primary causes. Apoptosis of lens epithelial cells (LECs) is considered the major cytological basis of many cataracts except congenital cataracts. The purpose of this study was to investigate whether diosmetin could reduce oxidative stress-induced damage to LECs, and explore its regulatory pathway. Lens epithelial cell line SRA01/04 was used as the object of study. Using ultraviolet B (UVB) and hydrogen peroxide (H 2 O 2 ) as sources of oxidative stress, the protective effects of diosmetin at different concentrations on cells were investigated, including inhibition of proliferation, apoptosis, and oxidative stress. Molecular docking was then used to predict the target proteins and validation was performed at the cellular and protein levels. The oxidative stress of SRA01/04 was induced by UVB and H 2 O 2 , and inhibition of proliferation and apoptosis were observed. Here, diosmetin has a dose-dependent cell-protecting effect. This effect is achieved by targeting the MEK2 protein and inhibiting the MAPK signaling. In conclusion, diosmetin reduces H 2 O 2 - and UVB-induced inhibition of SRA01/04 proliferation and apoptosis by reducing oxidative stress-induced activation of the MAPK pathway.
- Journal
- Bioengineered
- Publish Year
- 2022
- Experiment Subject
- Experiment Type
- Cell Experiment
- Phenotype Related
- Cataract; Cataracts; Ophthalmic Disease; Congenital Cataracts
- Paper Title Cn
- Paper Title En
- Diosmetin attenuates oxidative stress-induced damage to lens epithelial cells via the mitogen-activated protein kinase (MAPK) pathway
- Bilingual Status
- semi_complete