Protective Effect of Quercetin on Sodium Iodate-Induced Retinal Apoptosis through the Reactive Oxygen Species-Mediated Mitochondrion-Dependent Pathway

Autor: Meilin Wang, Hui-Wen Lin, Yai-Ping Hsiao, Min-Yen Hsu, Yi-Ju Lee, Shang-Chun Tsou, Yuan-Yen Chang, Ching-Chung Chen, Jer-An Lin
Jazyk: angličtina
Rok vydání: 2021
Předmět:
0301 basic medicine
Retinal Pigment Epithelium
Mitochondrion
quercetin
lcsh:Chemistry
chemistry.chemical_compound
Macular Degeneration
0302 clinical medicine
lcsh:QH301-705.5
Spectroscopy
bcl-2-Associated X Protein
chemistry.chemical_classification
human retinal pigment epithelium
Caspase 3
apoptosis
General Medicine
Computer Science Applications
Cell biology
Mitochondria
medicine.anatomical_structure
Poly(ADP-ribose) Polymerases
Signal Transduction
Iodates
Article
Catalysis
Retina
sodium iodate
Cell Line
Inorganic Chemistry
03 medical and health sciences
mitochondrial membrane potential
Retinal Diseases
medicine
Humans
Physical and Theoretical Chemistry
Outer nuclear layer
Molecular Biology
age-related macular degeneration
PI3K/AKT/mTOR pathway
Reactive oxygen species
Retinal pigment epithelium
Organic Chemistry
Retinal
030104 developmental biology
chemistry
Gene Expression Regulation
lcsh:Biology (General)
lcsh:QD1-999
Apoptosis
030221 ophthalmology & optometry
Reactive Oxygen Species
Zdroj: International Journal of Molecular Sciences, Vol 22, Iss 4056, p 4056 (2021)
International Journal of Molecular Sciences
Volume 22
Issue 8
ISSN: 1661-6596
1422-0067
Popis: Age-related macular degeneration (AMD) leads to gradual central vision loss and is the third leading cause of irreversible blindness worldwide. The underlying mechanisms for this progressive neurodegenerative disease remain unclear and there is currently no preventive treatment for dry AMD. Sodium iodate (NaIO3) has been reported to induce AMD-like retinal pathology in mice. We established a mouse model for AMD to evaluate the effects of quercetin on NaIO3-induced retinal apoptosis, and to investigate the pertinent underlying mechanisms. Our in vitro results indicated that quercetin protected human retinal pigment epithelium (ARPE-19) cells from NaIO3-induced apoptosis by inhibiting reactive oxygen species production and loss of mitochondrial membrane potential as detected by Annexin V-FITC/PI flow cytometry. We also evaluated the relative expression of proteins in the apoptosis pathway. Quercetin downregulated the protein expressions of Bax, cleaved caspase-3, and cleaved PARP and upregulated the expression of Bcl-2 through reduced PI3K and pAKT expressions. Furthermore, our in vivo results indicated that quercetin improved retinal deformation and increased the thickness of both the outer nuclear layer and inner nuclear layer, whereas the expression of caspase-3 was inhibited. Taken together, these results demonstrate that quercetin could protect retinal pigment epithelium and the retina from NaIO3-induced cell apoptosis via reactive oxygen species-mediated mitochondrial dysfunction, involving the PI3K/AKT signaling pathway. This suggests that quercetin has the potential to prevent and delay AMD and other retinal diseases involving NaIO3-mediated apoptosis.
Databáze: OpenAIRE
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