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Journal of Ophthalmology
Volume 2016 (2016), Article ID 8341439, 7 pages
Research Article

Effects of Lutein on Hyperosmoticity-Induced Upregulation of IL-6 in Cultured Corneal Epithelial Cells and Its Relevant Signal Pathways

1Department of Ophthalmology, Show Chwan Memorial Hospital, No. 526, Section 1, Zhongshan Road, Changhua 500, Taiwan
2Institute of Electrical and Computer Engineering, National Chiao Tung University, Hsinchu 30010, Taiwan
3Central Taiwan University of Science and Technology, No. 666, Buzih Road, Beitun District, Taichung 40601, Taiwan
4New York Eye and Ear Infirmary of Mount Sinai, 310 East 14th Street, New York, NY 10003, USA
5Department of Optometry, Yuan Pei University, Hsinchu 30015, Taiwan
6Department of Optometry, Chung Shan Medical University, Taichung 40201, Taiwan

Received 24 December 2015; Accepted 15 February 2016

Academic Editor: Qing-huai Liu

Copyright © 2016 Shih-Chun Chao et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Dry eye is a common disorder characterized by deficiency of tear. Hyperosmoticity of tear stimulates inflammation and damage of ocular surface tissues and plays an essential role in the pathogenesis of dry eye. Cultured human corneal epithelial (CE) cells were used for the study of effects of lutein and hyperosmoticity on the secretion of IL-6 by CE cells. Cell viability of CE cells was not affected by lutein at 1–10 μM as determined by MTT assay. Hyperosmoticity significantly elevated the secretion of IL-6 by CE cells as measured by ELISA analysis. The constitutive secretion of IL-6 was not affected by lutein. Lutein significantly and dose-dependently inhibited hyperosmoticity-induced secretion of IL-6. Phosphorylated- (p)- p38 MAPK, p-JNK levels in cell lysates and NF-κB levels in cell nuclear extracts were increased by being exposed to hyperosmotic medium. JNK, p38, and NF-κB inhibitors decreased hyperosmoticity-induced secretion of IL-6. Lutein significantly inhibited hyperosmoticity-induced elevation of NF-κB, p38, and p-JNK levels. We demonstrated that lutein inhibited hyperosmoticity-induced secretion of IL-6 in CE cells through the deactivation of p38, JNK, and NF-κB pathways. Lutein may be a promising agent to be explored for the treatment of dry eye.