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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 investigate the effect of m elaton in (MT) on the anti-oxidative injury in brain and the dose-effect relationship after traumatic brain injury (TBI) in rats. To explore the effect of MT as free Base scavenger against TB I oxidative damage may be the mechanism of the brain, providing experimental evidence for the clinical application of MT. Methods A traumatic brain injury model was established by free-fall impact injury. MT and vitamin C were injected intraperitoneally 5 m after injury, and glutathione peroxidase (GSH-Px) was measured in cerebral cortex of rats 2 h after injury (CAT) and malondialdehyde (MDA) contents were observed and ultrastructural changes were observed. Results After traumatic brain injury, the activity of GSH-Px, CAT decreased and the content of MDA increased. The early MT was able to partially counteract this change, and the greater the MT dose, the stronger the effect. Conclusion The early administration of MT after TBI can antagonize oxidative damage in the brain and protect the brain. The mechanism may be related to the protection of GSH-Px and CAT activity and the reduction of lipid peroxidation.