Neuroprotective effect of melatonin on retinal ganglion cells in rats

Abstract

To investigate the neuroprotective effect of melatonin (MT) on retinal ganglion cells (RGCs) in rats with ischemia reperfusion injury (RIR), 24 healthy SD rats were randomly divided into two groups: group A and group B. RIR model was induced in the left eyes by increasing the pressure of the anterior chamber. Group A was treated with 10 % alcohol- normal saline (1 mL/kg/d, ip), while group B was treated with 0.5 % MT (1 mL/kg/d, ip). On the basis of the time interval between the left eyes RIR and the sacrifice, rats in both group A and group B were further divided into 3 subgroups: groups A1 and B1 (days 7), groups A2 and B2 (days 14), groups A3 and B3 (days 30), with 4 rats in each subgroup. 7 day before the sacrifice, 3 % fluorogold was bilaterally injected into superior colliculi and geniculate body. The eyes were enucleated after being sacrificed, and mounting of the retina from both eyes was performed on a slide and observed under a fluorescence microscope. Four photos were taken from each of the four quadrants of the retina. The labeled-RGCs were counted by using a computerized image analyzer. The rate of the labeled-RGCs was used for statistical analysis. Our results showed that, in group A, the rate of the labeled-RGCs was (77.16 +/- 6.35) %, (65.53 +/- 7.01) %, (53.85 +/- 4.38) % on day 7, 14 and 30. In group B, the rate of the labeled-RGCs was (81. 33 +/- 9.27) %, (79.80 +/- 8.36) %, (80. 34 +/- 11.05) % on day 7, 14 and 30. In group B, which was treated with MT after RIR, the rate of labeled-RGCs was significantly higher than that of group A on day 14 and day 30 (P<0.05). It is concluded that, in the RIR rats, MT therapy could increase the survival rate of the RGCs and could rescue and restore the injured RGCs.

Circadian regulation of pineal gland rhythmicity

“…Increasing evidence support the role of NAS as an antioxidant, which is more effective than melatonin (reviewed in (Oxenkrug, 2005)). NAS was shown to protect against 6-hydroxydopamine-induced neurotoxicity (Aguiar et al, 2005) and against glutamine-induced lipid peroxidation in retinal samples (Tang et al, 2006). More recently, NAS was shown to activate TrkB (a receptor for brain derived neurotrophic factor – BDNF) leading to an antidepressant-like behavior (Jang et al, 2010).…”