Melatonin's Protective Effects on Neurons in an Cell Injury Model.

Background: Currently, the role of melatonin (MT) in neuronal damage remains unclear and this study aimed to explore the protective effects of MT on neurons in an cell injury model.

Methods: The Sprague Dawley (SD) rat traumatic brain injury (TBI) model was prepared, and brain tissue extract (BTE) from the injured area were generated. To establish a cell injury model , the BTE was added to the culture medium during the neuron culture process. MT was introduced into the culture medium of the cell injury model to observe its protective effects on neurons. Relevant molecular biology experiments were conducted to observe cellular oxidative stress status, inflammation, endoplasmic reticulum (ER) stress, mitochondrial damage, and neuronal apoptosis.

Results: When compared to the control group, the BTE group exhibited a significant increase in cellular oxidative stress, inflammation, neurofilament light polypeptide (NEFL) expression, and ER stress. Additionally, the mitochondrial DNA (mtDNA) copy number significantly decreased, and there was a higher count of apoptotic cells ( < 0.05). Upon the addition of MT to the culture medium of the in vitro cell injury model, there was a significant reduction in cellular oxidative stress, inflammation, and NEFL levels. This addition also mitigated ER stress, increased mtDNA copy numbers, and decreased the ratio of cell apoptosis ( < 0.05).

Conclusions: In the cell injury model, MT demonstrates the capacity to inhibit cellular oxidative stress, inflammation, and ER stress levels. Additionally, it diminishes mtDNA damage, fosters cell viability, and serves as a protective agent against both apoptosis and necrosis in neurons.