Immediate and delayed treatments with curcumin prevents forebrain ischemia-induced neuronal damage and oxidative insult in the rat hippocampus
Immediate and delayed treatments with curcumin prevents forebrain ischemia-induced neuronal damage and oxidative insult in the rat hippocampus
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DOI：
10.1007/s11064-006-9059-1
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发表时间：
2006-05-01
影响因子：
4.4
通讯作者：
Al-Majed, Abdulhakeem A.
中科院分区：
文献类型：
--
作者：
Al-Omar, Fadhel A.;Nagi, Mahmoud N.;Al-Majed, Abdulhakeem A.
氧化应激被认为是缺血性损伤后神经退行性变的原因之一。本研究旨在探讨姜黄素(Cur)对大鼠短暂性前脑缺血后海马CA1区神经元死亡可能的抗氧化性神经保护作用。Cur治疗(200 mg/kg/d，i.p)缺血后即刻、3h和24 h三个不同时间点(P<；0.01)均能显著减轻缺血7d后神经元的损伤。此外，Cur还能降低缺血大鼠体内升高的丙二醛水平，并使GSH含量、过氧化氢酶和超氧化物歧化酶活性恢复到正常水平。在体外，CuR与抗氧化剂(IC50=1 mU M)和丁基羟基甲苯一样有效。本研究表明，姜黄素治疗可减轻前脑缺血所致的神经元损伤和海马区组织的氧化应激反应。因此，即刻或延迟至24小时给予姜黄素治疗，有可能成为人类前脑缺血损伤的保护剂。
Oxidative stress is believed to contribute to neurodegeneration following ischemic injury. The present study was undertaken to evaluate the possible antioxidant neuroprotective effect of curcumin (Cur) on neuronal death of hippocampal CA1 neurons following transient forebrain ischemia in rat. Treatment of Cur (200 mg/kg/day, i.p.) at three different times (immediately, 3 h and 24 h after ischemia) significantly (P < 0.01) reduced neuronal damage 7 days after ischemia. Also, treatment of ischemic rats with Cur decreased the elevated levels of MDA and increased GSH contents, catalase and SOD activities to normal levels. In the in vitro, Cur was as potent as antioxidant (IC50 = 1 mu M) as butylated hydroxytoluene. The present study demonstrates that curcumin treatment attenuates forebrain ischemia-induced neuronal injury and oxidative stress in hippocampal tissue. Thus treatment with curcumin immediately or even delayed until 24 h may have the potential to be used as a protective agent in forebrain ischemic insult in human.