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Quercetin counteracts the cellular damage caused by HNE and inhibits inflammation in ARPE‐19 cells
Author(s) -
HYTTI M,
PIIPPO N,
SALMINEN A,
KAARNIRANTA K,
KAUPPINEN A
Publication year - 2013
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2013.4772.x
Subject(s) - inflammation , quercetin , p38 mitogen activated protein kinases , creb , oxidative stress , mapk/erk pathway , lipid peroxidation , lactate dehydrogenase , viability assay , 4 hydroxynonenal , pharmacology , chemistry , kinase , microbiology and biotechnology , immunology , biology , biochemistry , apoptosis , antioxidant , enzyme , gene , transcription factor
Purpose Age‐related macular degeneration(AMD) is the leading cause of blindness in the western world. And despite extensive research many questions about disease progression and formation still remain unanswered. One of the driving factors of AMD is a chronic inflammatory process, stimulated by life‐long exposure to light and oxidative stress. In the current study we try to evaluate the anti‐inflammatory properties of Quercetin, a plant derived polyphenol, and to determine the pathways by which it inhibits inflammation. Methods Cultured ARPE‐19 cells were treated with the lipid peroxidation endproduct 4‐Hydroxynonenal (HNE) to induce an inflammatory response. Quercetin was added 1 hour after stimulation with HNE to assess its power to suppress an already activated inflammatory response. The effects of the treatment on intracellular inflammation were measured with ELISA and quantitative Real‐Time PCR. Cell viability was assessed using the lactate dehydrogenase (LDH)‐assay. Results Our results show that Quercetin decreased the levels of the pro‐inflammatory cytokines MCP‐1 and IL‐8. It also protected the cells from HNE‐induced toxicity, as was evidenced by a decrease in LDH levels. Quercetin lowered the levels of mitogen‐activated protein kinase (MAP) p38 and of phospho‐CREB but did not affect the levels of NF‐κB or the DNA binding efficacy of its subunit p65. Conclusion Our results show that Quercetin can reduce the inflammatory response in retinal pigment epithelial cells by down regulating the MAPK pathway and decreasing the phosphorylation of CREB. Furthermore it is able to protect cells from death induced by oxidative stress. Quercetin may, therefore, be a valuable tool in the therapy of inflammation in AMD.