Melatonin regulates traumatic optic neuropathy via targeting autophagy.

OBJECTIVE

Traumatic optic neuropathy (TON) usually refers to the indirect damage to the optical nerve, which can cause partial or complete blindness. Melatonin (MT) is a kind of indole hormone, and the retina is one of its natural sites of secretion in the human body. This study aims to explore MT in the retina and optic nerve injuries due to TON.

MATERIALS AND METHODS

Sprague-Dawley (SD) rats were used for TON model in the study. After operation, rats were treated with MT or phosphate buffered saline (PBS) for 4, 7, 14, 21, and 28 days before sacrifice. The changes in retinal ganglion cells (RGCs) were observed via hematoxylin-eosin (HE) staining. Terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) staining was applied to observe apoptosis. Immunofluorescence staining was applied to detect caspase-3 and Western blot was used to detect LC3, cleaved caspase-3 and glyceraldehyde phosphate dehydrogenase (GAPDH).

RESULTS

The number of RGCs in MT group increased compared to the model group. After MT treatment, the increased number of TUNEL positive cells and the increased number of caspase-3 positive cells in the retina of MT group was alleviated. Moreover, Western blot analysis revealed that the LC3-II/LC3-I ratio in the retinal tissue of MT group was further increased, while the increased cleaved caspase-3 protein level in the retina of MT group was alleviated compared to the model group.

CONCLUSIONS

The results of this study revealed that MT therapy affects the apoptosis level of RGCs after TON through alleviating the increased caspase-3 protein level. Its mechanism may be that it further up-regulates the autophagy level of RGCs after TON, ultimately inhibiting the apoptosis of RGCs after TON and playing a neuroprotective role.