Caffeic acid phenethyl ester lessens disease symptoms in an experimental autoimmune uveoretinitis mouse model. (May 2015)

• Record Type: Journal Article
• Authors: Choi, Jae-Hyeog; Roh, Kug-Hwan; Oh, Hana; Park, Sol-Ji; Ha, Sung-Min; Kang, Mi Seon; Lee, Ji-Hyun; Jung, So Young; Song, Hyunkeun; Yang, Jae Wook; Park, SaeGwang
• Is Part Of: Experimental eye research. Volume 134(2015:May)
• Page Start: 53
• Page End: 62
• Publication Date: 2015-05
• Subjects: Experimental autoimmune uveoretinitis -- Caffeic acid phenethyl ester -- Interphotoreceptor retinal-binding protein -- Pro-inflammatory cytokine -- Nuclear factor-kappa B; Ophthalmology -- Periodicals; Eye -- Periodicals; Œil -- Périodiques; Ophthalmology; Periodicals; Electronic journals; 612.8405
• DOI: 10.1016/j.exer.2015.03.014
• Languages: English
• ISSNs: 0014-4835

Abstract

Abstract: Experimental autoimmune uveoretinitis (EAU) is an autoimmune disease that models human uveitis. Caffeic acid phenethyl ester (CAPE), a phenolic compound isolated from propolis, possesses anti-inflammatory and immunomodulatory properties. CAPE demonstrates therapeutic potential in several animal disease models through its ability to inhibit NF-κB activity. To evaluate these therapeutic effects in EAU, we administered CAPE in a model of EAU that develops after immunization with interphotoreceptor retinal-binding protein (IRBP) in B10.RIII and C57BL/6 mice. Importantly, we found that CAPE lessened the severity of EAU symptoms in both mouse strains. Notably, treated mice exhibited a decrease in the ocular infiltration of immune cell populations into the retina; reduced TNF-α, IL-6, and IFN-γ serum levels: and inhibited TNF-α mRNA expression in retinal tissues. Although CAPE failed to inhibit IRBP-specific T cell proliferation, it was sufficient to suppress cytokine, chemokine, and IRBP-specific antibody production. In addition, retinal tissues isolated from CAPE-treated EAU mice revealed a decrease in NF-κB p65 and phospho-IκBα. The data identify CAPE as a potential therapeutic agent for autoimmune uveitis that acts by inhibiting cellular infiltration into the retina, reducing the levels of pro-inflammatory cytokines, chemokine, and IRBP-specific antibody and blocking NF-κB pathway activation. Highlights: Caffeic acid phenethyl ester lessens disease symptoms in EAU mouse model. Caffeic acid phenethyl ester alters the ocular infiltrating cell population. Caffeic acid phenethyl ester regulates the cytokine and chemokine. Caffeic acid phenethyl ester inhibits NF-κB pathway activation.