Effect of Melatonin on Expression of c-Jun Proteins and BDNF mRNA in Transient Global Ischemia-Reperfusion Injury of Rat Brain

No, Yong Hwan; Wi, Dai Han; Park, Jae Hwang

Abstract

PURPOSE: The purpose of this study was to investigate the effect of systemic treatment of melatonin known as a potent free radical scavenger on expression of c-Jun proteins and brain-derived neurotrophic factor (BDNF) mRNA in transient global ischemia-reperfusion injury of rat brain.
METHODS
Spargue-Dalwey rats were used and divided into three groups: ischemia group, ischemia group pretreated with melatonin, ischemia group posttreated with melatonin. Brain ischemia-reperfusion injury induced by occlusion of bilateral carotid and vertebral arteries (4-vessel occlusion) for 15 min followed by recirculation of cerebral blood flow. Animals were received intraperitoneal injection of melatonin (10 mg/kg) either 30 min before ischemia (pretreatment) or 0 min after reperfusion (posttreatment). Four vessel occlusion-reperfusion produced ischemic injury in major forebrain structures such as striatum, cortex, hippocampus in the finding of triphenyltetrazolium chloride (TTC) staining. Spectrophotometric assay for formazan, an end-product of TTC showed increased value of formazan formation in ischemic area of the brain posttreated with melatonin 24 hours after the ischemia-reperfusion injury.
RESULTS
Posttreatment with melatonin caused a significant decreased in number of c-Jun immunoreactive neurons in CA1 region of the hippocampus after ischemia-reperfusion insult. Furthermore, autoradiographic density for BDNF mRNA in the hippocampus and cortex was increased by systemic treatment with melatonin especially in posttreatment group.
CONCLUSION
These results suggest that melatonin treatment results in an attenuation of ischemic damage caused by ischemia-reperfusion in nueronal cells of the sensitive areas of rat brain.