NDLI: Doxycycline Attenuates Endotoxin-Induced Uveitis by Prostaglandin E2-EP4 Signaling.

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Doxycycline Attenuates Endotoxin-Induced Uveitis by Prostaglandin E2-EP4 Signaling.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Han, Longhui Huang, Jingwen Cheng, Xiaokang Dai, Ye Chen, Xiaoqing Su, Wenru Liang, Dan
Description	Country affiliation: China Author Affiliation: Huang J ( State Key Laboratory of Ophthalmology Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China 2Department of Ophthalmology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.); Su W ( State Key Laboratory of Ophthalmology Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China.); Chen X ( State Key Laboratory of Ophthalmology Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China.); Cheng X ( State Key Laboratory of Ophthalmology Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China.); Dai Y ( State Key Laboratory of Ophthalmology Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China.); Han L ( State Key Laboratory of Ophthalmology Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China.); Liang D ( State Key Laboratory of Ophthalmology Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China.)
Abstract	PURPOSE: We explored the anti-inflammatory effects of doxycycline in experimental uveitis and the underlying mechanisms. METHODS: Rats with endotoxin-induced uveitis (EIU) received doxycycline (1.5 mg/kg) or the control vehicle via intraperitoneal injection. Clinical scores were graded under a slit lamp. Rat peritoneal macrophages were used in vitro to further explore the anti-inflammatory mechanisms of doxycycline. The levels of nitric oxide (NO), TNF- , IL-1ß, prostaglandin E2 (PGE2), cyclooxygenase (COX)-2, I kappa B- (IκB- ), inducible nitric oxide synthase (iNOS), Akt, caspase-3, and nuclear factor-kappa B (NF-κB) were analyzed. RESULTS: Treatment with doxycycline dramatically reduced the clinical scores of EIU (P < 0.001), with significant decreases in inflammatory cell infiltration, protein concentrations, and the production of NO, TNF- , and IL-1ß in the aqueous humor (AqH). In vitro, doxycycline significantly inhibited the production of NO, IL-1ß, and TNF- in peritoneal macrophages by modulating the PI3K/Akt/IκB- /NF-κB pathway. Importantly, we found that doxycycline significantly enhanced COX2 expression and PGE2 production both in vivo and in vitro. More importantly, blockade of the EP4 receptor of PGE2 significantly reversed the doxycycline-mediated inhibition of macrophages and the PI3K/Akt pathway in vitro. Furthermore, simultaneous injection of an EP4 antagonist and doxycycline significantly blocked the doxycycline-mediated attenuation of EIU. CONCLUSIONS: Doxycycline can ameliorate EIU, and PGE2-EP4 signaling is essential for the anti-inflammatory effects of doxycycline in vitro and in vivo.
ISSN	01460404
e-ISSN	15525783
Journal	Investigative Opthalmology & Visual Science
Issue Number	11
Volume Number	56
Language	English
Publisher	Association for Research in Vision and Ophthalmology
Publisher Date	2015-10-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Anti-inflammatory Agents Therapeutic Use Dinoprostone Physiology Doxycycline Uveitis Drug Therapy Animals Aqueous Humor Chemistry Caspase 3 Cyclooxygenase 2 Endotoxins Pharmacology I-kappa B Proteins Macrophages Drug Effects Nf-kappa B Nitric Oxide Synthase Nitric Oxide Synthase Type Ii Nitroglycerin Proto-oncogene Proteins C-akt Rats, Wistar Receptors, Prostaglandin E, Ep4 Subtype Signal Transduction Slit Lamp Chemically Induced Research Support, Non-u.s. Gov't Discipline Ophthalmology
Content Type	Text
Resource Type	Article
Subject	Ophthalmology Sensory Systems Cellular and Molecular Neuroscience

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