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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
Objective To investigate the protective effect of melatonin (MT) on acute cerebral ischemia-reperfusion injury and its mechanism. Methods The rat model of acute middle cerebral artery occlusion (MCAO) injury was established by thread occlusion. The contents of malondialdehyde (MDA), superoxide dismutase (SOD) And myeloperoxidase (MPO) activity, as well as the levels of thromboxane B2 (TXB2) and 6 keto prostaglandin F1α (6-keto PGF1α) in plasma. Results MT 10,2 0 mg · kg -1 could protect the activity of SOD and decrease the level of MDA in brain tissue, and the level of TXB2 and 6-keto PGF1α in plasma could be restored by 20 mg · kg -1, high. Conclusion The protective effect of MT on acute cerebral ischemia-reperfusion injury in rats is related to the increase of antioxidant enzyme activity, anti-lipid peroxidation and anti-inflammatory effects