The therapeutic effects of melatonin and nimodipine in rats after cerebral cortical injury

Turk Neurosurg. 2012;22(6):740-6. doi: 10.5137/1019-5149.JTN.6197-12.1.


Aim: Secondary brain injury starts after the initial traumatic impact and marked by an increase in the intracellular calcium concentrations.This cascadeeventually results in membrane lipid peroxidation and neuronal cell death.

Material and methods: We investigated the neuro-protective effects of nimodipine and melatonin in 38 rats after 6 hours of head trauma using the cortical impact injury model of Marmarou.

Results: Brain water in the melatonin-given group decreased significantly comparing to that of control group the brain water in the nimodipine given group increased significantly comparing to that of trauma group. Histopathologically, brain edema was significantly low in melatonin-administered group comparing to that of control group while there were no changes in brain edema in the nimodipine given group and in the group that both nimodipine and melatonin were administered in combination. MDA levels in the brain tissues were significantly lower in the melatonin and nimodipine groups comparing to those of trauma and control group however this difference was by far significant in melatonin group comparing to nimodipine group.

Conclusion: Melatonin appears to have neuro-protective effects on the secondary brain damage while nimodipine and nimodipine plus melatonin combination did not show such neuro-protective effects on the secondary brain injury.

MeSH terms

  • Animals
  • Brain / drug effects
  • Brain Edema / drug therapy*
  • Brain Injuries / drug therapy*
  • Disease Models, Animal
  • Drug Combinations
  • Lipid Peroxidation / drug effects
  • Male
  • Melatonin / pharmacology*
  • Neuroprotective Agents / pharmacology*
  • Nimodipine / pharmacology*
  • Rats
  • Rats, Sprague-Dawley


  • Drug Combinations
  • Neuroprotective Agents
  • Nimodipine
  • Melatonin