Oral administration of melatonin modulates the expression of tumor necrosis factor-α (TNF-α) gene in irradiated rat cervical spinal cord

Abstract

Aim

We aimed to determine the changes in TNF-α expression and Malondialdehyde (MDA) level in a short time after irradiation. Furthermore, we evaluated the effect of melatonin on the modulation of TNF-α gene expression.

Background

The radio-sensitivity of the cervical spinal cord limits the dose of radiation which can be delivered to tumors in the neck region. There is increasing evidence that TNF-α has a role in the development of the acute phase of spinal cord injury.

Materials/Methods

Four groups of rats were investigated. Group 1 (vehicle treatment) served as the control. Group 2 (radiation) was treated with the vehicle, and 30[[ce:hsp sp="0.25"/]]min later, the rats were exposed to radiation. Group 3 (radiation[[ce:hsp sp="0.25"/]]+[[ce:hsp sp="0.25"/]]melatonin) was given an oral administration of melatonin (100[[ce:hsp sp="0.25"/]]mg/kg body weight) and 30[[ce:hsp sp="0.25"/]]min later exposed to radiation in the same manner as in group 2. Group 4 (melatonin-only) was also given an oral administration of melatonin (100[[ce:hsp sp="0.25"/]]mg/kg body weight). 5[[ce:hsp sp="0.25"/]]mg/kg of melatonin was administered daily to rats in groups 3 and 4, and the vehicle was administered daily to rats in groups 1 and 2.

Results

Three weeks after irradiation, TNF-α gene up-regulated almost 5 fold in the irradiated group compared to the normal group. TNF-α gene expression in the melatonin pretreatment group, compared to the radiation group, was significantly down-regulated 3 weeks after irradiation (p[[ce:hsp sp="0.25"/]]<[[ce:hsp sp="0.25"/]]0.05). MDA levels increased after irradiation and then significantly decreased under melatonin treatment.

Conclusion

We suggest that inhibition of TNF-α expression by oral administration of melatonin may be a therapeutic option for preventing radiation-induced spinal cord injury.