Abstract
Green tea extract (GTE) ingested by rats exerted anti-oxidative activities in various ocular tissues as shown in our previous studies. The present work investigated anti-inflammatory effects of GTE on endotoxin-induced uveitis (EIU). EIU was generated in adult rats by a footpad injection of 1 mg/kg lipopolysaccharide (LPS). Oral administration of GTE (550 mg/kg) was given one, two or four times after LPS injection. Twenty-four hours later, LPS produced severe hyperemia and edema in the iris. Immunocytochemical examinations showed an accumulation of infiltrating cells in the aqueous humor that were immunopositive for cluster of differentiation 43 (CD43) and CD68, markers for leucocytes and macrophages, respectively. Analyses of the aqueous humor showed an increase in pro-inflammatory mediators including tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and monocyte chemoattractant protein-1 (MCP-1). GTE treatments improved the clinical manifestations and reduced infiltrating cells and protein exudation in the aqueous humor, which were not observed under half dose of GTE (275 mg/kg). The number of CD68 positive macrophages residing in the iris and ciliary was also reduced. GTE suppressed production of TNF-α, IL-6 and MCP-1 in the aqueous humor, which was associated with a down-regulation of LPS receptor complex subunits, Toll-like receptor 4 (TLR-4) and CD14, and suppression of nuclear factor-kappa Bp65 (NF-κBp65) in the iris and ciliary body. Our findings show that GTE is a potent anti-inflammatory agent against the inflammation of EIU, and suggest a potential use in treatment of acute uveitis.
Highlights
Uveitis, an ocular inflammatory condition, accounts for approximately 10–15% cases of total blindness and up to 20% of legal blindness in developed world [1,2]
The major findings include: i) Green tea extract (GTE) alleviates clinical manifestations of ocular inflammation; ii) it reduces infiltration of leukocytes and macrophages, and leakage of protein into aqueous humor and vitreous body; iii) it suppresses production of pro-inflammatory biomarkers tumor necrosis factor-a (TNF-a), IL-6 and monocyte chemoattractant protein-1 (MCP-1) in aqueous humor; iv) these anti-inflammatory effects are associated with down-regulation of LPS receptors, Toll-like receptor 4 (TLR-4) and CD14, and reduction of nuclear NF-kBp65, v) GTE reduces accumulation of macrophages in the stroma of iris and ciliary body
We have shown in this study that the levels of pro-inflammatory mediators, TNF-a, IL-6 and MCP-1, were elevated significantly in the aqueous humor twenty-four hours after LPS injection
Summary
An ocular inflammatory condition, accounts for approximately 10–15% cases of total blindness and up to 20% of legal blindness in developed world [1,2]. The rat model of endotoxin-induced uveitis (EIU) has been widely used for evaluating potential ocular anti-inflammatory compounds since it was reported in 1980 [7,8,9,10,11,12]. It has been reported that LPS was recognized by membrane-bound cluster of differentiation 14 (mCD14) and Toll-like receptors (principally TLR-4) on the surface of macrophages. Receptors activation in these immune surveillance cells resulted in phosphorylation of nuclear factor-kappa B (NF-kB) and caused release of pro-inflammatory factors, such as tumor necrosis factor-a (TNF-a), interlukin-6 (IL-6) and monocyte chemoattractant protein-1 (MCP-1) [15,16,17,18,19,20,21]. The inflammatory process reaches peak level at 18–24 hours after LPS injection [27]
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