EGCG protects against UVB-induced apoptosis via oxidative stress and the JNK1/c-Jun pathway in ARPE19 cells
Open accessAbstract
Ultraviolet B (UVB) radiation is part of the spectrum of light produced by the sun. This form of radiation has been implicated as one of the potential etiological factors causing age-related macular degeneration (AMD). Oxidative injury to the retinal pigment epithelium (RPE) has also been thought to play a key role in AMD. The aim of the present study was to determine the mechanism by which UVB causes damage to the RPE cells, whether it occurs through oxidative stress and the mitogen-activated protein kinase (MAPK) pathway and whether the green tea extract, (-)-epigallocatechin gallate (EGCG), has a protective role. Cell viability assays were used to determine the viability of the cells under different conditions. Cell death caused by apoptosis was determined using fluorescein isothiocyanate conjugated-annexin V/PI labeling, followed by flow cytometry. Intracellular reactive oxygen species (ROS) levels were measured by flow cytometry. Western blot analysis was used to detect UVB-induced MAPK signaling pathways. The findings showed that UVB induced apoptosis, which increased intracellular ROS in ARPE19 cells. Inhibition of c-Jun NH2-terminal kinase (JNK) with a specific inhibitor augmented this apoptosis, and anisomycin (an activator of JNK) attenuated this apoptosis. In addition, UVB decreased the phosphorylation of JNK1 and c-Jun. Finally, EGCG reduced the ROS generation and apoptosis, and also partially blocked the decreased phosphorylation of JNK1 and c-Jun by UVB irradiation. The findings show that UVB irradiation is able to induce apoptosis in ARPE19 cells through oxidative stress, but EGCG treatment attenuates this damage. In this situation, the JNK pathway plays an anti-apoptotic role. The use of selective activators or antioxidants may be useful in reducing the oxidative damage occurring in AMD.
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JNK activation has an anti-apoptotic role in UVA-induced damage in RPE cells.
“and they implicate an “anti-apoptotic role” of JNK activation in this context [ 40 ].”
From MAPK Pathways in Ocular Pathophysiology: Potential Therapeutic Drugs and Challenges (2023) · cites this paper as [40]
The Results section ('Inhibition of JNK augments UVB-induced ARPE19 cell apoptosis') reports that JNK activation reduced apoptosis in ARPE19 cells. The claim changes the exposure from UVB to UVA; our copy does not establish the anti-apoptotic role under UVA exposure. (LLM, conf=0.91)
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- Authors
- Jiang, Q.
- Affiliations
- Nanjing Medical University (CN)
- Corresponding author
- Jiang, Qin
- ORCID
- Jiang, Qin
- Venue
- Molecular Medicine Reports
- Publisher
- Spandidos Publications
- Published
- 2011-09-09
- Volume
- 5
- Issue
- 1
- Pages
- 54-9
- ISSN
- 1791-2997 (ISSN-L)
- 1791-3004
- OpenAlex
- W2057243273
- Cited by
- 59
- References
- 27
- Citations by year
- 2025: 1 · 2024: 5 · 2023: 4 · 2022: 4 · 2021: 2 · 2020: 5 · 2019: 3 · 2018: 8 · 2017: 6 · 2016: 5 · 2015: 1 · 2014: 5 · 2013: 6 · 2012: 4
- FWCI
- 4.49
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Molecular Medicine Reports (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Government of Jiangsu Province
- Topics
- Health Sciences › Medicine › Ophthalmology › Retinal Diseases and Treatments
- Health Sciences › Medicine › Dermatology › Skin Protection and Aging
- Health Sciences › Medicine › Ophthalmology › Ocular and Laser Science Research
- Keywords
- epigallocatechin gallate, UV-B radiation, apoptosis, oxidative stress, retinal pigment epithelium, ARPE-19 cells, age-related macular degeneration, reactive oxygen species, MAPK signaling, green tea extract, anisomycin
- MeSH terms
- Anisomycin, Anti-Bacterial Agents, Catechin, Cell Line, Epithelial Cells, Humans, Phosphorylation, Ultraviolet Rays, Apoptosis, Reactive Oxygen Species, Oxidative Stress, MAP Kinase Signaling System, JNK Mitogen-Activated Protein Kinases, Mitogen-Activated Protein Kinase 8
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