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A. Manola, G. Trichonas, Y. Morizane, S. Montezuma, X. Koufomichali, Y. Murakami, A. Thanos, D. Vavvas; AICAR (5-Aminoimidazole-4-Carboxamide-1-Beta-D-Ribofuranoside) Ameliorates Inflammation in the Endotoxin Induced Uveitis Model. Invest. Ophthalmol. Vis. Sci. 2010;51(13):5235.
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To evaluate the effect of intravitreal injection of 5-Aminoimidazole-4-carboxamide ribonucleoside (AICAR) on experimental uveitis. AICAR is an activator of AMP-activated protein kinase (AMPK) and has been reported to have antiinflammatory and immunomodulatory effects in various models of inflammation. We investigated whether AICAR modulates the inflammatory reaction/inflammation in endotoxin-induced uveitis (EIU) in mice.
C57BL/6J mice were divided randomly into three groups. EIU was induced by intravitreal injections of lipopolysaccharide (LPS). Group 1 (n=6) received intravitreal injection of normal saline, group 2 (n=14) received intravitreal injection of 1 microg Salmonella typhimurium endotoxin and group 3 (n=14) animals received intravitreal injection of 1 microg Salmonella typhimurium endotoxin plus AICAR (1mM). Inflammation was evaluated by clinical examinations on day 1 after injection, by measuring the vascular permeability using a biotinylated albumin method and by measuring the mRNA levels of proinflammatory mediators 6 hrs after injection. (IL-6, TNF-a, MCP-1).
No inflammation occurred in the control group (group 1). Eyes of animals treated with LPS and AICAR had significantly less intraocular inflammation than animals treated with LPS alone. AICAR treatment decreased LPS induced vascular permeability three fold (p<0.05) as well as expression of proinflammatory mediators in the retina.
Intravitreal injection of AICAR suppresses ocular inflammation in a mouse model of severe endotoxin-induced uveitis.
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