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Kazuichi Maruyama, Hiroshi Keino, Kotaro Yamamoto, Satoru Moritoh, Toru Nakazawa; Prevention of Experimental Autoimmune Uveitis by Inhibition of the Cyclooxigenaze-2-Linked Pathway in a Rodent Model. Invest. Ophthalmol. Vis. Sci. 2014;55(13):98.
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© ARVO (1962-2015); The Authors (2016-present)
Uveitis is the one of the leading causes of blindness worldwide. It has been reported that current treatments for uveitis associated with autoimmune or idiopathic diseases rely on steroid or immunosuppressive medication. However, treatment with steroid or immunosuppressive medication leads to many complications. The purpose of the present study was to investigate new medications for uveitis treatment that do not lead to severe complications.
Male Lewis rats (6-8 weeks old) were used in all experiments. As an experimental model of autoimmune uveoritinitis (EAU), the rats received an injection into one hind footpad of R14 (0.5 mg) in 0.1 ml emulsion and 5 ml of complete Freund’s adjuvant. Killed B pertussis suspension was then administered intraperitoneally as an additional adjuvant. Simultaneously, the rats received 500 ppm (4 mg/kg) cyclo-oxigenase (COX)-2 inhibitor orally every day. At 21 days after immunization, the rats were euthanized and evaluated both histologically and for clinical score. Additionally, inflammatory cytokine mRNAs were assessed in the retina.
COX-2 inhibitor treatment was found to suppress inflammation both clinically (p=0.019, n=10) and histologically (p=0.0203, n=5). Moreover, the COX-2 inhibitor was able to suppress the activation in the retina of inflammatory cytokines, such as TNF-alpha (p=0.0041) and interferon-gamma (p=0.0130).
The findings of the present study show that COX-2 inhibitors have the ability to suppress EAU. Further development of COX-2 inhibitors may reveal them to be new candidate drugs for the treatment of uveitis.
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