Melatonin regulates traumatic optic neuropathy via targeting autophagy

Area of Science:

• Neuroscience
• Ophthalmology
• Pharmacology

Background:

• Traumatic optic neuropathy (TON) can lead to vision loss due to indirect optic nerve damage.
• Melatonin (MT), a hormone secreted in the retina, is being investigated for its therapeutic potential.
• Understanding MT's role in TON is crucial for developing new treatments.

Purpose of the Study:

• To investigate the effects of Melatonin (MT) on retinal ganglion cells (RGCs) and optic nerve injury in a rat model of TON.
• To explore the underlying mechanisms of MT's neuroprotective action in TON.

Main Methods:

• A traumatic optic neuropathy (TON) model was established in Sprague-Dawley rats.
• Rats were treated with MT or PBS, with observations at 4, 7, 14, 21, and 28 days post-treatment.
• Retinal ganglion cell (RGC) counts, apoptosis (TUNEL, caspase-3), and autophagy markers (LC3) were assessed using HE staining, immunofluorescence, and Western blot.

Main Results:

• MT treatment increased the number of retinal ganglion cells (RGCs) compared to the control group.
• MT alleviated apoptosis by reducing TUNEL-positive and caspase-3-positive cells in the retina.
• MT enhanced autophagy (increased LC3-II/LC3-I ratio) and reduced cleaved caspase-3 levels.

Conclusions:

• Melatonin (MT) demonstrates neuroprotective effects in traumatic optic neuropathy (TON).
• MT therapy alleviates RGC apoptosis by modulating caspase-3 levels.
• Upregulation of autophagy may be a key mechanism for MT's neuroprotective role in TON.