褪黑激素為強而有效之自然抗氧化劑與自由基攔截劑，先前的研究已於急性缺血性腦中風發現褪黑激素具備強而有效之神經保護效果。本研究利用缺血性腦中風老鼠模式，做出可逆轉的中大腦動脈縫線栓塞S.D.品系大白鼠，探討褪黑激素對缺血性腦中風治療後之短期追蹤，評估其神經保護特性，與其神經再塑的潛能。對可逆轉中大腦動脈縫線栓塞後第7天，應用Nissl法染色腦切片以及影像處理系統計算之栓塞大小；並以西方墨點法分析突觸傷害指標( SNAP-25、Synaptophysin )及軸索生長指標( GAP43 )的蛋白表現。實驗結果顯示，在缺血60分之後，以褪黑激素進行緩慢靜脈注射，由免疫組織化學染色可觀察到，在腦部缺血／再灌流之後，cortical infarction以及striatal infarction的體積，和控制組比對有降低的現象，顯示褪黑激素有助於灰質損傷的降低。另外藉由西方墨點法之結果觀察得知，在右側（大腦動脈阻塞側）的皮質半影區，與皮質缺氧中心區域的 SNAP-25、synaptophysin，以及 GAP43蛋白表現，於實驗組相對於對照組均有增加。由此顯示褪黑激素除具有神經保護弁鄍~，也具備有神經再塑的潛力。本研究證實了褪黑激素具有神經保護及神經再塑的潛力。 Melatonin is a well known free radical scavenger and antioxidant supplement. It has been suggested that strong neuroprotection following transient focal cerebral ischemia. This study aim at invesgitation of the neuroplasticity potential of melatonin following transient focal cerebral ischemia in rats. Reversible transient middle cerebral artery occlusion in Sprague-Dawley rat is our stroke model. Delayed intravenous administration of melatonin ( 5 mg/ kg ) at 60 minutes after ischemia. A series of experiment evaluated neuroprotection and neuroplasticity effects after stroke rats treated melatonin. Postmortem infarct volumes will be determined by quantitative image analysis of Nissl-stained brain sections. Synaptic damage markers ( SNAP-25, synaptophysin ) and axon growth marker ( GAP43 ) protein expression was evaluated by western blot methods. Nissl-stained brain sections in melatonin treated cerebral ischemia-reperfusion rats shows reduction of cortical and striatal infarction. This result support melatonin could reduce grey matter damage. Western blot in synaptic damage markers and axon growth marker protein shows melatonin could improve penumbra and ischemic core of ischemic brain. All of the results suggest melatonin have the potential of neuroprotection and neuroplasticity.
