Protective Effects of 7S,15R-Dihydroxy-16S,17S-Epoxy-Docosapentaenoic Acid (diHEP-DPA) against Blue Light-Induced Retinal Damages in A2E-Laden ARPE-19 Cells

被引:0
|
作者
Song, Seung-Yub [1 ,2 ]
Park, Dae-Hun [3 ]
Lee, Sung-Ho [1 ,2 ]
Lim, Han-Kyu [2 ,4 ]
Park, Jin-Woo [1 ,2 ]
Seo, Jeong-Woo [5 ]
Cho, Seung-Sik [1 ,2 ]
机构
[1] Mokpo Natl Univ, Coll Pharm, Dept Pharm, Muan 58554, Jeonnam, South Korea
[2] Mokpo Natl Univ, Coll Pharm, Biomed Hlth & Life Convergence Sci, BK21 Four, Muan 58554, Jeonnam, South Korea
[3] Dongshin Univ, Coll Oriental Med, Naju Si 58245, Jeonnam, South Korea
[4] Mokpo Natl Univ, Dept Marine & Fisheries Resources, Muan 58554, Jeonnam, South Korea
[5] Korea Res Inst Biosci & Biotechnol KRIBB, Microbial Biotechnol Res Ctr, Jeongeup Si 56212, Jeonbuk Do, South Korea
基金
新加坡国家研究基金会;
关键词
docosahexaenoic acid; diHEP-DPA; blue light; eye health; ARPE-19; MACULAR DEGENERATION; OXIDATIVE STRESS; ACUTE-INFLAMMATION; INDUCED APOPTOSIS; RESOLUTION; MECHANISMS; ACTIVATION; RESOLVINS; MEDIATORS; DEATH;
D O I
10.3390/antiox13080982
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The purpose of this study was to investigate the protective effects of 7S,15R-dihydroxy-16S,17S-epoxy-docosapentaenoic acid (diHEP-DPA) in retinal pigment epithelial (RPE) cell damage. ARPE-19 cells, a human RPE cell line, were cultured with diHEP-DPA and Bis-retinoid N-retinyl-N-retinylidene ethanolamine (A2E), followed by exposure to BL. Cell viability and cell death rates were determined. Western blotting was performed to determine changes in apoptotic factors, mitogen-activated protein kinase (MAPK) family proteins, inflammatory proteins, and oxidative and carbonyl stresses. The levels of pro-inflammatory cytokines in the culture medium supernatants were also measured. Exposure to A2E and BL increased the ARPE-19 cell death rate, which was alleviated by diHEP-DPA in a concentration-dependent manner. A2E and BL treatments induced apoptosis in ARPE-19 cells, which was also alleviated by diHEP-DPA. Analysis of the relationship with MAPK proteins revealed that the expression of p-JNK and p-P38 increased after A2E and BL treatments and decreased with exposure to diHEP-DPA in a concentration-dependent manner. DiHEP-DPA also affected the inflammatory response by suppressing the expression of inflammatory proteins and the production of pro-inflammatory cytokines. Furthermore, it was shown that diHEP-DPA regulated the proteins related to oxidative and carbonyl stresses. Taken together, our results provide evidence that diHEP-DPA can inhibit cell damage caused by A2E and BL exposure at the cellular level by controlling various pathways involved in apoptosis and inflammatory responses.
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页数:17
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