Abstract
To evaluate the effects of 1% morphine instillation on clinical parameters, aqueous humor turbidity, and expression levels of tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1beta), prostaglandin E2 (PGE2), and myeloperoxidase (MPO) in rabbits with endotoxin-induced experimental uveitis. Twenty four New Zealand white rabbits were divided into four groups (n=6 each): control (CG), morphine (MG), naloxone (NG), and morphine-naloxone (MNG) groups. Under dissociative anesthesia, 0.1 mL of solution containing 0.2 µg of lipopolysaccharide (LPS) endotoxin from the Salmonella typhimurium cell wall was injected in the vitreous chamber. Clinical evaluations (conjunctical hyperemia, chemosis blepharospasm, and ocular discharge) and laser flaremetry were performed before (baseline), and 10 and 20 hours after induction of uveitis. Rabbits were subsequently euthanized and eyes were enucleated to quantify expression levels of TNF-α, IL-1 beta, PGE2, and MPO. No significant differences in clinical parameters and flare values were observed between the study groups. TNF-α and IL-1 beta levels increased significantly in the CG, MG, NG, and MNG groups compared to baseline (P<0.05). Significant differences in PGE2 levels were observed between the MG and NMG groups (P<0.05). A trend toward increased MPO activity was observed in response to uveitis induction; however, this trend did not reach statistical significance (P>0.05). Morphine has no effect on clinical parameters, flare, or expression levels of inflammatory mediators in a rabbit model of uveitis induced by intravitreal injection of LPS.
Highlights
Uveitis is defined as inflammation of the uveal tract and has been shown to be associated with a number intraocular diseases, including cataract[1,2,3]
The present study aimed to evaluate the effects of morphine instillation on rabbit eyes with uveitis
Uveitis induction resulted in increased expression of TNF-α and IL-1 beta (Table 1)
Summary
Uveitis is defined as inflammation of the uveal tract and has been shown to be associated with a number intraocular diseases, including cataract[1,2,3]. Acute inflammatory responses in uveitis are maintained by the action of molecular mediators which leads to decreased active secretion of aqueous humor and increased vascular permeability[6,7]. Pro-inflammatory cytokines, such as interleukin-1 alpha (IL-1 alpha) and interleukin-1 beta (IL-1 beta), have been shown to actively recruit leukocytes to sites of inflammation[6]. IL-1 alpha and IL-1 beta are predominantly secreted by activated macrophages, B lymphocytes, and endothelial cells[8]. Tumor necrosis factor-alpha (TNF-α) is synthesized by monocytes, macrophages, neutrophils, mast cells, Submitted for publication: March 23, 2015 Accepted for publication: September 14, 2015
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
