褪黑素对癫痫大鼠海马氧化应激及神经元凋亡的影响

发布时间：2018-03-17 00:18

本文选题：癫痫　切入点：褪黑素　出处：《中国康复理论与实践》2016年05期 　论文类型：期刊论文

【摘要】：目的探讨褪黑素对癫痫大鼠海马氧化应激及神经元凋亡的影响及其机制。方法成年雄性Sprague-Dawley大鼠72只等分为对照组、模型组、褪黑素低剂量组和褪黑素高剂量组。模型组侧脑室注射马桑内酯50μg/kg,褪黑素低、高剂量组分别于腹腔注射褪黑素20 mg/kg和60 mg/kg后30 min,侧脑室注射马桑内酯50μg/kg。癫痫持续60 min后,采用紫外分光光度计检测丙二醛(MDA)、超氧化物歧化酶(SOD)的含量;原位末端标记法(TUNEL法)检测大鼠海马CA3区神经元凋亡;电镜观察海马CA3区神经元及其线粒体改变。结果与对照组相比,模型组海马神经元、线粒体出现明显超微结构损伤,凋亡细胞数显著增多(P0.001),海马SOD显著降低(P0.001),MDA显著升高(P0.001)。与模型组相比,褪黑素低剂量组大鼠海马神经元、线粒体超微结构损伤有所改善,凋亡细胞数明显减少(P0.01),SOD升高(P0.05),MDA降低(P0.05);褪黑素高剂量组大鼠海马神经元、线粒体超微结构损伤明显改善,凋亡细胞数显著减少(P0.001),且与对照组相比无显著性差异(P0.05),SOD显著升高(P0.001),MDA显著降低(P0.001)。结论给予外源性褪黑素可明显减少癫痫大鼠海马神经元凋亡,高剂量效果更佳,其作用机制可能涉及褪黑素对抗氧化应激反应,减轻神经元、线粒体损伤。
[Abstract]:Objective to investigate the effect and mechanism of melatonin on oxidative stress and neuronal apoptosis in hippocampus of epileptic rats. Methods 72 adult male Sprague-Dawley rats were divided into control group and model group. Low dose group and high dose group of melatonin, 50 渭 g / kg cortisone and low melatonin were injected into the lateral ventricle of the model group. The high dose group was injected with melatonin for 20 mg/kg and 60 mg/kg respectively, and the lateral ventricle was injected with cortisone 50 渭 g / kg. The epilepsy lasted 60 min. The contents of malondialdehyde (MDA) and superoxide dismutase (SOD) were detected by ultraviolet spectrophotometer, and the apoptosis of neurons in CA3 region of rat hippocampus was detected by in situ end labeling method (Tunel). The changes of neurons and mitochondria in hippocampal CA3 region were observed by electron microscope. Results compared with the control group, the model group showed obvious ultrastructural damage in hippocampal neurons and mitochondria. The number of apoptotic cells increased significantly (P 0.001) and the SOD of hippocampus decreased significantly (P 0.001). Compared with the model group, the damage of ultrastructure of mitochondria was improved in melatonin low-dose group. The number of apoptotic cells decreased significantly, SOD increased, MDA decreased, and the ultrastructure damage of mitochondria was significantly improved in the high dose group of melatonin. Compared with the control group, the number of apoptotic cells decreased significantly, and there was no significant difference in the number of apoptotic cells. Compared with the control group, there was no significant difference in the number of apoptotic cells. Compared with the control group, the SOD of P0. 05 was significantly increased and the MDA of P0. 001 was significantly decreased. Conclusion exogenous melatonin can significantly reduce the apoptosis of hippocampal neurons in epileptic rats, and the high dose of melatonin has a better effect. The mechanism may be involved in melatonin to antioxidant stress response, reduce neuronal, mitochondrial damage.
【作者单位】：发育与再生四川省重点实验室;成都医学院人体解剖与组织胚胎学教研室;四川大学华西医院西藏成办分院;
【基金】：发育与再生四川省重点实验室基金(No.SYS10-005) 成都医学院校基金(No.CYZ14-009)
【分类号】：R742.1

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