摘要
目的研究大鼠创伤性脑损伤(traum atic brain in jury,TB I)后早期给予褪黑素(m elaton in,MT)对脑内抗氧化损伤的作用以及作用的量效关系;探讨MT作为自由基清除剂对抗TB I后脑内氧化损伤可能的机制,为MT的临床应用提供实验依据。方法采用自由落体撞击伤方法制作创伤性脑损伤模型,致伤后5m in腹腔注射MT及维生素C,测定脑损伤后2h大鼠大脑皮层谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)及丙二醛(MDA)含量并观察超微结构的变化。结果创伤性脑损伤后大脑皮层GSH-Px,CAT活性降低,MDA含量升高,通过早期给予MT能部分对抗这种变化,且MT剂量越大,作用越强。结论大鼠TB I后早期给予MT可以对抗脑内的氧化损伤,有脑保护作用,其机制可能与保护GSH-Px、CAT活性,减少脂质过氧化有关。
Objective To study the therapy of melatonin on rat brain cortex oxidated trauma after following traumatic brain injury and the relation of quantity and effect. Methods Seventy - two Sprague - Dawley rats were put into experiment and divided into six groups of 12 rats each. Traumatic brain injury has been developed through Feeney＇ s method. MT and VC was given intraperitoneal （ i. p. ） after being injuried 5 minutes and determined the activities of GSH - Px and CAT and the content of MDA in rat brain cortex after 2 hours following TBI. The ultrastructure in brain cortex was also been examined. Results The activeties of of GSH - Px and CAT reduced in rat brain cortex following traumatic brain injury, but content of MDA rose. MT early treatment can partly reverse thses changes, and the more much MT was used, the more obviously effect on reducing the brain edema can be observed. Conclusions Melatonin was found to resist brain cortex oxidated trauma and be neuroprotective in instances of traumatic brain injury, its probable mechanism is related to protect the activities of GSH - Px and CAT. Thus , melatonin may be a valuable therapeutic agent in the treatment of TBI.
出处
《锦州医学院学报》
2006年第3期27-30,共4页
Journal of Jinzhou Medical College
