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二十二碳六烯酸對Pentylenetetrazol(PTZ)誘發大鼠癲癇造成神經膠細胞凋亡作用及空間記憶之影響

Effect of Docosahexaenoic Acid on Apoptosis of Glial Cells and Spatial Learning in Rats with Pentylenetetrazole-induced Epileptic Seizure

摘要


In the present study, we investigated the beneficial effects of docosahexaenoic acid (DHA) supplementation on detriments in central nervous system (CNS) by using pentylenetetrazol (PTZ)-induced seizure in neonatal rats as an animal model. To prove this hypothesis, we induced seizure attacks on ten-day-old post-natal (P10) rats and examining their glial cells' apoptosis and spatial learning before or after treated with 0.4% fish oil (FO) or corn oil (CO). In experiment 1 (Exp 1), the dietary treatment was undertaken on the same day as PTZ-induced seizure until animals were sacrificed for examining the protection of DHA in fish oil from the brain injury in PTZ-induced seizure. Meanwhile, the prevention effect of fish oil on CNS damage was evaluated by giving the dietary treatment for consecutive 7 days before PTZ-induced seizure in experiment 2 (Exp 2). The results showed significant increases of DHA percentages in phospholipids of brain tissue and decreased apoptosis of oligodendrocytes and microglia cells in FO in Exp 1 (p<0.05). The percentages of DHA were negatively correlated with the apoptosis of oligodendrocytes in Exp 1 (r=-0.61, p=0.02). The mean percentage of total swimming time in target region as escape latency in FO tended to be longer than that in CO in both of Exp 1 and 2. These results implicate that DHA protects the glial cells from apoptosis in brain injury caused by PTZ-induced seizure and thus improves special learning activities.

並列摘要


In the present study, we investigated the beneficial effects of docosahexaenoic acid (DHA) supplementation on detriments in central nervous system (CNS) by using pentylenetetrazol (PTZ)-induced seizure in neonatal rats as an animal model. To prove this hypothesis, we induced seizure attacks on ten-day-old post-natal (P10) rats and examining their glial cells' apoptosis and spatial learning before or after treated with 0.4% fish oil (FO) or corn oil (CO). In experiment 1 (Exp 1), the dietary treatment was undertaken on the same day as PTZ-induced seizure until animals were sacrificed for examining the protection of DHA in fish oil from the brain injury in PTZ-induced seizure. Meanwhile, the prevention effect of fish oil on CNS damage was evaluated by giving the dietary treatment for consecutive 7 days before PTZ-induced seizure in experiment 2 (Exp 2). The results showed significant increases of DHA percentages in phospholipids of brain tissue and decreased apoptosis of oligodendrocytes and microglia cells in FO in Exp 1 (p<0.05). The percentages of DHA were negatively correlated with the apoptosis of oligodendrocytes in Exp 1 (r=-0.61, p=0.02). The mean percentage of total swimming time in target region as escape latency in FO tended to be longer than that in CO in both of Exp 1 and 2. These results implicate that DHA protects the glial cells from apoptosis in brain injury caused by PTZ-induced seizure and thus improves special learning activities.

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