The effect of melatonin on apoptosis due to experimental traumatic brain damage on rats

Scope: This in our study we tried to demonstrate the distribution of indicators of apoptosis in time and location in rats to which we performed experimental focal head trauma. We also tried to demonstrate the decrease of apoptosis indicators by giving melatonin and we searched the effect of oxidative stress on post traumatic apoptosis.Material and Method: We divided the rats into four groups as control, trauma, trauma+melatonin, trauma+placebo. And then we divided each group into five subgroups. The rats were sacrificed after 12, 24, 72, 120 and 168. hours. We observed the distribution of apoptosis indicators caspase 3, caspase 8, and matrix metalloproteinase 9 in time and location. Results: In our study we also observed that as in many physiopathological processes oxidative stress and apoptosis act togather in post traumatic secondary brain injury and we also observed that oxidative stress contributes apoptosis by inducting MMP-9 pathway except caspas, but we also observed that immunoreactives only effect the traumatic hemisphere and don't effect the opposite site. We demonstrated that the immuno reaction and apoptosis in traumatic hemisphere reaches peak level at 24 hours and rapidly slows down after 72 hours but doesn't reach zero level. In the rats given melatonin to decrease oxidative stress thus apoptosis, the indicators of apoptosis significantly decrease but doesn't reach zero level.Conclusion: To our results we concluded that melatonin is one of the most important agents to prevent posttraumatic secondary damage due to oxidative stress-induced apoptosis but further studies are needed fowsing on melatonin as a single or a polytherapeutic agent.Key Words: Head injury, oxidative stress, apoptosis, caspase, melatonin, matrix mettalloprotein