Abstract：
It is to investigate the effects of β-asarone on learning and memory, hippocampal morphology, synaptophysin (SYP) and postsynaptic density 95(PSD95) protein expression, N-methyl-D-aspartic acid receptor 2B (NR2B)- Ca2+/calmodulin (CaM)-dependent protein kinase II (CaMKII) - Extracellular signal-regulated kinase (ERK) / Cyclic-AMP response element binding protein (CREB) signal in hippocampus of rats with exhaustive exercise-induced fatigue.
Fifty Sprague-Dawley male rats were randomly divided into five groups: normal group, exercise group, exercise and β-asarone (2.5, 10, 40 mg/kg)-treated groups. The learning and memory in rats were tested by Morris water maze experiment. We measured the hippocampal morphology by Nissl staining. The levels of SYP, PSD95, NR2B, CaMKII, ERK1/2, CREB, p-NR2B, p-CaMKII, p-ERK1/2 and p-CREB expression were measured by western blot analysis.
The results demonstrated that β-asarone (10, 40 mg/kg) treatment significantly decreased the latency to find the platform, increased the time spent in the target quadrant and the number of crossing the platform of rats with exhaustive exercise-induced fatigue. β-asarone (10, 40 mg/kg) treatment increased the cell density in the hippocampus CA1 region, significantly up-regulated NR2B-CaMKII-ERK/CREB signal and improved the protein expression levels of SYP and PSD95 in hippocampus of rats with exhaustive exercise-induced fatigue.
It suggests that β-asarone could improve learning and memory of rats with exhaustive exercise-induced fatigue. The mechanism might be related to β-asarone protecting the morphology of hippocampus, increasing the protein expression levels of SYP and PSD95 and up-regulating NR2B-CaMKII-ERK/CREB signal in hippocampus of rats with exhaustive exercise-induced fatigue.
Fifty Sprague-Dawley male rats were randomly divided into five groups: normal group, exercise group, exercise and β-asarone (2.5, 10, 40 mg/kg)-treated groups. The learning and memory in rats were tested by Morris water maze experiment. We measured the hippocampal morphology by Nissl staining. The levels of SYP, PSD95, NR2B, CaMKII, ERK1/2, CREB, p-NR2B, p-CaMKII, p-ERK1/2 and p-CREB expression were measured by western blot analysis.
The results demonstrated that β-asarone (10, 40 mg/kg) treatment significantly decreased the latency to find the platform, increased the time spent in the target quadrant and the number of crossing the platform of rats with exhaustive exercise-induced fatigue. β-asarone (10, 40 mg/kg) treatment increased the cell density in the hippocampus CA1 region, significantly up-regulated NR2B-CaMKII-ERK/CREB signal and improved the protein expression levels of SYP and PSD95 in hippocampus of rats with exhaustive exercise-induced fatigue.
It suggests that β-asarone could improve learning and memory of rats with exhaustive exercise-induced fatigue. The mechanism might be related to β-asarone protecting the morphology of hippocampus, increasing the protein expression levels of SYP and PSD95 and up-regulating NR2B-CaMKII-ERK/CREB signal in hippocampus of rats with exhaustive exercise-induced fatigue.
摘要：
目的：探讨β-细辛脑对学习记忆的影响,海马形态，突触素（SYP）和突触后密度95（PSD95）蛋白表达，N-甲基-D-天冬氨酸受体2B(NR2B)-Ca2+/钙调蛋白(CaM)依赖性蛋白激酶II(CaMKII)-细胞外信号调节激酶(ERK)/环AMP反应元件结合蛋白(CREB)信号在力竭运动性疲劳大鼠海马中的表达.方法：雄性SD大鼠50只,随机分为5组:正常组,运动组,运动和β-细辛脑（2.5、10、40mg/kg）治疗组。通过Morris水迷宫实验测试大鼠的学习记忆能力。我们通过Nissl染色测量了海马形态。SYP的水平，PSD95,NR2B,CaMKII,ERK1/2,CREB,p-NR2B,p-CaMKII,通过蛋白质印迹分析测量p-ERK1/2和p-CREB表达。结果：β-细辛脑(10,40mg/kg)治疗明显缩短了寻找平台的潜伏期,增加了运动性疲劳大鼠在目标象限的时间和穿越平台的数量。β-细辛脑(10,40mg/kg)处理增加海马CA1区细胞密度,显著上调NR2B-CaMKII-ERK/CREB信号,提高力竭运动性疲劳大鼠海马SYP和PSD95蛋白表达水平。结论：β-细辛醚能改善力竭运动性疲劳大鼠的学习记忆能力。其机制可能与β-细辛脑保护海马形态有关,提高力竭运动性疲劳大鼠海马SYP和PSD95蛋白表达水平,上调NR2B-CaMKII-ERK/CREB信号。
