【摘要】 目的　探讨褪黑素 (melatonin ,MT)对急性脑缺血再灌注损伤的保护作用及机制。方法　用线栓法制备大鼠大脑中动脉急性缺血再灌注损伤模型 ,再灌注 2 4h后测定大鼠脑组织中丙二醛 (malondialdehyde ,MDA)含量、超氧化物歧化酶 (superoxidedismutase,SOD)和髓化过氧化物酶(myeloperoxidaseMPO)活性以及血浆中血栓素B2 (throm boxaneB2 ,TXB2 )、6 酮 前列腺素F1α( 6 keto prostaglandinF1α,6 酮 PGF1α)含量。结果　MT 10、2 0mg·kg-1能保护SOD活性、减缓脑组织中MDA的升高 ,2 0mg·kg-1还可恢复血浆中TXB2 与 6 酮 PGF1α的平衡 ,减缓脑组织中MPO的升高。结论　MT对大鼠急性脑缺血再灌注损伤的保护作用与其提高抗氧化酶活性 ,抗脂质过氧化损伤及抗炎作用有关更多还原

【Abstract】 AIM To study the protective effects of melatonin(MT) on acute cerebral ischemia reperfusion injury.METHODS The model of cerebral ishemia-2 h/reperfusion-24 h was induced by middle cerebral artery occlusion(MCAO) in SD rats. Melatonin (10,20 mg·kg -1 ip)was administered four times in an animal:At 0, 1, 2, 6 h of reperfusion. After 24 h reperfusion, the content of malondialdehyde(MDA),the activities of superoxide dismutase(SOD)and myeloperoxidase (MPO)in brain tissue, the content of thromboxane B 2(TXB 2) and 6-keto-prostaglandin F 1α(6-keto-PGF 1α)in plasma were measured. RESULTS Compared with vehicle group, MT 10, 20 mg·kg -1 protected the activity of SOD, reduced the content of MDA, MT 20 mg·kg -1 also inhibited the increase of MPO in brain tissue ,and attenuated the disequilibrium of TXB 2 /6-keto-PGF 1α.CONCLUSION The protective effects of MT on acute cerebral ischemia reperfusion injury may be related to its increasing antioxidase activities,decreasing lipid peroxidative damage and inhibiting inflammations.更多还原