Melatonin as a Therapeutic Resource for Inflammatory Visual Diseases

被引:15
作者
Aranda, Marcos L. [1 ]
Gonzalez Fleitas, Maria Florencia [1 ]
Dieguez, Hernan [1 ]
Iaquinandi, Agustina [1 ]
Sande, Pablo H. [1 ]
Dorfman, Damian [1 ]
Rosenstein, Ruth E. [1 ]
机构
[1] Univ Buenos Aires, CONICET, Lab Retinal Neurochem & Expt Ophthalmol, Dept Human Biochem,Sch Med,CEFyBO, Paraguay 2155,5th Floor, RA-1121 Buenos Aires, DF, Argentina
关键词
Melatonin; uveitis; optic neuritis; ocular inflammation; oxidative damage; nitrosative damage; ENDOTOXIN-INDUCED UVEITIS; NITRIC-OXIDE SYNTHASE; ACUTE OPTIC NEURITIS; MITOCHONDRIAL OXIDATIVE STRESS; LIPID-PEROXIDATION; PINEAL-GLAND; RAT RETINA; VITAMIN-E; CIRCADIAN REGULATION; MULTIPLE-SCLEROSIS;
D O I
10.2174/1570159X15666170113122120
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Background: Uveitis and optic neuritis are prevalent ocular inflammatory diseases, and highly damaging ocular conditions. Both diseases are currently treated with corticosteroids, but they do not have adequate efficacy and are often associated with severe side effects. Thus, uveitis and optic neuritis remain a challenging field to ophthalmologists and a significant public health concern. Objective: This review summarizes findings showing the benefits of a treatment with melatonin in experimental models of these inflammatory ocular diseases. Results: Oxidative and nitrosative damage, tumor necrosis factor, and prostaglandin production have been involved in the pathogeny of uveitis and optic neuritis. Melatonin is an efficient antioxidant and antinitridergic, and has the ability to reduce prostaglandin and tumor necrosis factor levels both in the retina and optic nerve. Moreover, melatonin not only prevents functional and structural consequences of experimental uveitis and optic neuritis, but it is also capable of suppressing the actively ongoing ocular inflammatory response. Conclusions: Since melatonin protects ocular tissues against inflammation, it could be a potentially useful anti-inflammatory therapy in ophthalmology.
引用
收藏
页码:951 / 962
页数:12
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