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(Investigative Ophthalmology and Visual Science. 2007;48:5013-5022.)
© 2007 by The Association for Research in Vision and Ophthalmology, Inc.
DOI:  10.1167/iovs.07-0393
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Emodin Suppression of Ocular Surface Inflammatory Reaction

Ai Kitano,1 Shizuya Saika,1 Osamu Yamanaka,1 Kazuo Ikeda,2 Yuka Okada,1 Kumi Shirai,1 and Peter S. Reinach3

1From the Department of Ophthalmology, Wakayama Medical University, Wakayama, Japan; the 2Department of Anatomy, Graduate School of Medicine, Osaka City University, Osaka, Japan; and the 3State University of New York College of Optometry, New York, New York.

PURPOSE. To determine whether a Chinese herbal medicine component, emodin, suppresses inflammatory/fibrogenic reaction in cultured subconjunctival fibroblasts and reduces injury-induced increases in ocular surface inflammation in mice.

METHODS. Effects of emodin were measured in human subconjunctival fibroblasts on proliferation and migration with colorimetry and scratch wound assay, respectively. Neovascularization was evaluated using an endothelial cell-fibroblast coculture model. Proinflammatory mediator and extracellular matrix component gene and protein expression was characterized with real-time reverse transcription-polymerase chain reaction, enzyme immunoassay, and immunocytochemistry, respectively. Western blotting and immunohistochemistry evaluated the activation of nuclear factor-{kappa}B (NF-{kappa}B) and c-Jun N-terminal kinase (JNK). In a mouse corneal alkali-burn model, the effects of emodin on ocular surface inflammation and fibrosis were evaluated.

RESULTS. Emodin suppressed tumor necrosis factor {alpha} (TNF-{alpha})-induced fibroblast migration and fibronectin deposition in vitro. VEGF induced neovascularization but did not affect cell proliferation and collagen type 1 production. Monocyte/macrophage-chemoattractant protein-1 gene and protein expression declined. Emodin inhibited TNF-{alpha}-induced NF-{kappa}B p65 and JNK activation but did not affect transforming growth factor ß1-induced Smad2/3 signaling. In vivo, emodin inhibited proinflammatory and fibrogenic reactions.

CONCLUSIONS. Emodin suppressed in vitro TNF-{alpha}-induced stimulation of proinflammatory reaction. In a mouse ocular alkali burn model, this herbal component lessened inflammation and scarring. Additional studies are warranted to evaluate the therapeutic potential of emodin in lessening ocular tissue inflammation and resultant fibrosis after injury.




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M. Iribarne, V. Torbidoni, K. Julian, J. P. Prestifilippo, D. Sinha, V. Rettori, A. Berra, and A. M. Suburo
Cannabinoid Receptors in Conjunctival Epithelium: Identification and Functional Properties
Invest. Ophthalmol. Vis. Sci., October 1, 2008; 49(10): 4535 - 4544.
[Abstract] [Full Text] [PDF]


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