Melatonin as an ocular anti-inflammatory

Abstract

Uveitis is a prevalent intraocular inflammatory disease, and one of the most damaging ocular conditions. Currently available therapies are relatively effective in the treatment of uveitis, but are often associated with severe side effects. In that context, uveitis remains a challenging field to ophthalmologists and represents a significant public health concern. Oxidative stress-induced inflammation is a major contributor to uveitis. In addition, altered nitric oxide (NO) metabolism, and increased prostaglandins (PGs) and tumor necrosis factorα (TNFα) levels also play a significant role in the pathogenesis of uveitis. Therefore, an antioxidant and anti-nitridergic therapy, as well as reducing PG and TNFα levels may be useful strategies to diminish tissue damage and ocular dysfunction induced by uveitis. Several lines of evidence strongly support that melatonin is a potent antioxidant molecule which is effective in scavenging free radicals that are generated in ocular tissues, and that it is able to reduce the retinal nitridergic pathway activity along with PG and TNFα levels. In view of the fact that melatonin lacks significant adverse collateral effects even at high doses, the application of melatonin could potentially protect ocular tissues by effectively scavenging free radicals, and reducing excessive amounts of NO, PGs, and TNFα generated in the uveitic eye. This chapter summarizes recent investigations showing that melatonin not only prevents clinical, biochemical, histological, ultrastructural, and functional consequences of experimental uveitis, but it is also capable of suppressing the actively ongoing ocular inflammatory response. These results strongly support the role of melatonin as a therapeutic strategy for uveitis treatment.