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Silibinin treatment prevents endotoxin-induced uveitis in rats in vivo and in vitro
Uveitis, an intraocular inflammatory disease, occurs mostly in young people and can result in the loss of socioeconomic capabilities. Silibinin has been shown to exert anti-inflammatory effects in human retinal pigment epithelial (RPE) cells. The present study investigated the anti-inflammatory effe...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5380317/ https://www.ncbi.nlm.nih.gov/pubmed/28376126 http://dx.doi.org/10.1371/journal.pone.0174971 |
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author | Chen, Ching-Long Chen, Jiann-Torng Liang, Chang-Min Tai, Ming-Cheng Lu, Da-Wen Chen, Yi-Hao |
author_facet | Chen, Ching-Long Chen, Jiann-Torng Liang, Chang-Min Tai, Ming-Cheng Lu, Da-Wen Chen, Yi-Hao |
author_sort | Chen, Ching-Long |
collection | PubMed |
description | Uveitis, an intraocular inflammatory disease, occurs mostly in young people and can result in the loss of socioeconomic capabilities. Silibinin has been shown to exert anti-inflammatory effects in human retinal pigment epithelial (RPE) cells. The present study investigated the anti-inflammatory effect of silibinin pretreatment on endotoxin-induced uveitis (EIU) in rats and the mechanisms by which it exerts these effects. Uveitis was induced via injection of lipopolysaccharides (LPS) into Lewis rats. Twenty-four hours after the LPS injection, histological examination showed that silibinin decreased inflammatory cell infiltration in the anterior segment of the eyes of LPS-treated rats. Analyses of the aqueous humor showed that silibinin decreased cell infiltration, protein concentration, nitric oxide (NO), and prostaglandin (PG)-E2 production. Western blot analysis indicated that silibinin decreased the expression of inducible NO synthase (iNOS), cyclooxygenase (COX-2), and phosphorylated IkB in the iris-ciliary body (ICB). Immunohistochemistry showed that silibinin decreased intercellular adhesion molecule (ICAM-1) expression in the ICB. In addition, western blot analysis showed that silibinin attenuated the expression of iNOS, COX-2, ICAM-1, and nuclear p65 in LPS-treated RAW cells. In conclusion, silibinin pretreatment prevents EIU and the subsequent production of proinflammatory mediators and ICAM-1, at least in part, by blocking the NF-κB–dependent signaling pathway both in vivo and in vitro. These effects may contribute to the silibinin-mediated preventive effects on intraocular inflammatory diseases such as acute uveitis. |
format | Online Article Text |
id | pubmed-5380317 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-53803172017-04-19 Silibinin treatment prevents endotoxin-induced uveitis in rats in vivo and in vitro Chen, Ching-Long Chen, Jiann-Torng Liang, Chang-Min Tai, Ming-Cheng Lu, Da-Wen Chen, Yi-Hao PLoS One Research Article Uveitis, an intraocular inflammatory disease, occurs mostly in young people and can result in the loss of socioeconomic capabilities. Silibinin has been shown to exert anti-inflammatory effects in human retinal pigment epithelial (RPE) cells. The present study investigated the anti-inflammatory effect of silibinin pretreatment on endotoxin-induced uveitis (EIU) in rats and the mechanisms by which it exerts these effects. Uveitis was induced via injection of lipopolysaccharides (LPS) into Lewis rats. Twenty-four hours after the LPS injection, histological examination showed that silibinin decreased inflammatory cell infiltration in the anterior segment of the eyes of LPS-treated rats. Analyses of the aqueous humor showed that silibinin decreased cell infiltration, protein concentration, nitric oxide (NO), and prostaglandin (PG)-E2 production. Western blot analysis indicated that silibinin decreased the expression of inducible NO synthase (iNOS), cyclooxygenase (COX-2), and phosphorylated IkB in the iris-ciliary body (ICB). Immunohistochemistry showed that silibinin decreased intercellular adhesion molecule (ICAM-1) expression in the ICB. In addition, western blot analysis showed that silibinin attenuated the expression of iNOS, COX-2, ICAM-1, and nuclear p65 in LPS-treated RAW cells. In conclusion, silibinin pretreatment prevents EIU and the subsequent production of proinflammatory mediators and ICAM-1, at least in part, by blocking the NF-κB–dependent signaling pathway both in vivo and in vitro. These effects may contribute to the silibinin-mediated preventive effects on intraocular inflammatory diseases such as acute uveitis. Public Library of Science 2017-04-04 /pmc/articles/PMC5380317/ /pubmed/28376126 http://dx.doi.org/10.1371/journal.pone.0174971 Text en © 2017 Chen et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Article Chen, Ching-Long Chen, Jiann-Torng Liang, Chang-Min Tai, Ming-Cheng Lu, Da-Wen Chen, Yi-Hao Silibinin treatment prevents endotoxin-induced uveitis in rats in vivo and in vitro |
title | Silibinin treatment prevents endotoxin-induced uveitis in rats in vivo and in vitro |
title_full | Silibinin treatment prevents endotoxin-induced uveitis in rats in vivo and in vitro |
title_fullStr | Silibinin treatment prevents endotoxin-induced uveitis in rats in vivo and in vitro |
title_full_unstemmed | Silibinin treatment prevents endotoxin-induced uveitis in rats in vivo and in vitro |
title_short | Silibinin treatment prevents endotoxin-induced uveitis in rats in vivo and in vitro |
title_sort | silibinin treatment prevents endotoxin-induced uveitis in rats in vivo and in vitro |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5380317/ https://www.ncbi.nlm.nih.gov/pubmed/28376126 http://dx.doi.org/10.1371/journal.pone.0174971 |
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