Abstract：
Melatonin is a powerful endogenous antioxidant hormone. Its healing effects on energy balance and neuronal damage associated with oxidative metabolism disorders have been reported in pathologic conditions. We aimed to determinate the utility of melatonin on neuronal damage, synaptic transmission, and energy balance in the brain tissue of rats with sepsis induced with LPS. Rats was divided into four groups such as control, LPS (20 mg/kg i.p.), melatonin (10 mg/kg i.p. × 3), and LPS + Melatonin (LPS + Mel). After 6 h from the first injection, rats were decapitated, and also tissue and serum samples were taken. Lipid peroxidation and neuron-specific enolase (NSE) levels were determined from the serum in all group. High energy compounds, creatine, and creatine phosphate are measured by HPLC methods from the homogenized tissue. Counts of living neurons are marked with NeuN (neuronal nuclei), degenerated neurons are marked with S100-ß and synaptic vesicles transmission is analyzed with synaptophysin antibodies immunoreactivities. One-way ANOVA and post hoc Tukey tests were used to statistical analysis. In LPS group, AMP, ATP, creatine, and creatine phosphate levels were significantly decreased (p < 0.05), and also ADP levels were significantly increased compared with the other groups (p < 0.01). Living neurons counts were significantly decreased in LPS (p < 0.01), melatonin, and LPS + Melatonin (p < 0.05) groups compared with control. Degenerated neurons counts were increased in LPS group compared with control (p < 0.01) and also decreased in both of melatonin and LPS + Melatonin groups (p < 0.01). Synaptophysin immunoreactivity was decreased in LPS group compared with the other groups (p < 0.05). We observed that melatonin administration prevents neuronal damage, regulates energy metabolism, and protects synaptic vesicle proteins from sepsis-induced reduction.
摘要：
褪黑素是一种强大的内源性抗氧化激素。已在病理条件下报道了其对能量平衡和与氧化代谢紊乱相关的神经元损伤的愈合作用。我们的目的是确定褪黑素对神经元损伤的效用，突触传递,LPS诱导脓毒症大鼠脑组织能量平衡。大鼠分为对照组等四组,LPS（20mg/kgi.p.），褪黑激素（10mg/kg腹膜内注射×3），和LPS+褪黑素(LPS+Mel)。从第一次注射开始6小时后，老鼠被斩首，并采集组织和血清样本。从所有组的血清中确定脂质过氧化和神经元特异性烯醇化酶（NSE）水平。高能化合物,肌酸,和磷酸肌酸通过HPLC方法从匀浆组织中测量。活神经元计数用NeuN（神经元核）标记，用S100-β标记退化的神经元，用突触素抗体免疫反应性分析突触小泡传递。采用单因素方差分析和事后Tukey检验进行统计分析。LPS组,AMP,ATP,肌酸,磷酸肌酸水平显著下降(p<0.05)，与其他组相比，ADP水平也显着升高（p<0.01）。LPS组存活神经元计数显著降低(p<0.01),褪黑激素,和LPS+褪黑素组(p<0.05)与对照组相比。与对照组相比，LPS组的变性神经元计数增加（p<0.01），而褪黑素和LPS褪黑素组的变性神经元计数也降低（p<0.01）。与其他组相比，LPS组的突触素免疫反应性降低（p<0.05）。我们观察到褪黑激素的给药可以防止神经元损伤，调节能量代谢，并保护突触囊泡蛋白免受脓毒症诱导的还原。
