In study,we investigated the effect of treatment with combination of walnut peptides with molecular weight<3 kDa and ginsenoside Rg1(<3 kDa+Rg1)on scopolamine-induced cognitive impairment in mice and the mechani...In study,we investigated the effect of treatment with combination of walnut peptides with molecular weight<3 kDa and ginsenoside Rg1(<3 kDa+Rg1)on scopolamine-induced cognitive impairment in mice and the mechanism of brain-derived neurotrophic factor(BDNF)/tyrosine kinase B(TrKB)/cAMP response element-binding protein(CREB)signaling pathway in PC12 cells.In behavioral experiments,<3 kDa+Rg1 treatment improved the memorizing ability of mice.Treatment with<3 kDa+Rg1 significantly regulated the function of neurotransmitters and effectively improved the morphology of the neurons determined by hematoxylin and eosin(H&E),Nissl,and Golgi staining.Additionally,immunohistochemistry showed that the<3 kDa+Rg1 treatment significantly decreased acetylcholinesterase(AChE)activity and increased choline acetyl transferase(ChAT)content in the hippocampus.The treatment upregulated vesicular acetylcholine transporter(VAChT),activated the BDNF/TrKB/CREB signaling pathway,improved the remodeling of dendritic spines,and enhanced cholinergic functions.In the scopolamine-induced PC12 cells,combination treatment increased thioredoxin-1(Trx-1)expression after administering TrKB and activated signaling pathway.The results showed combination of<3 kDa+Rg1 activated the BDNF/TrKB/CREB signaling pathway by regulating function of neurotransmitters and enhanced cholinergic function to decrease cognitive impairment.展开更多
研究石菖蒲和α-细辛醚抵抗大鼠疲劳运动后学习记忆下降的RGS14/MEK/ERK信号通路作用机制。80只SD大鼠按完全随机法分为:正常组(normal,Nor)、运动组(exercise,E)、运动+石菖蒲组(exercise+Acorus tatarinowii Schott,EAT)、运动+α-细...研究石菖蒲和α-细辛醚抵抗大鼠疲劳运动后学习记忆下降的RGS14/MEK/ERK信号通路作用机制。80只SD大鼠按完全随机法分为:正常组(normal,Nor)、运动组(exercise,E)、运动+石菖蒲组(exercise+Acorus tatarinowii Schott,EAT)、运动+α-细辛醚组(exercise+α-asarone,EαA)、运动+石菖蒲+RGS14拮抗剂CCG-63802组(EATC)、运动+α-细辛醚+RGS14拮抗剂CCG-63802(EαAR)、运动+石菖蒲+MEK拮抗剂U0126组(EATU)、运动+α-细辛醚+MEK拮抗剂U0126组(EαAU),每组10只。开展水迷宫实验进行学习记忆检测;利用免疫组化、免疫印迹(Western blot)和荧光实时定量PCR(RT-PCR)等方法检测G蛋白信号调节蛋白14(regulator of G protein signaling 14,RGS14)、Raf-1、磷酸化丝裂原活化蛋白激酶激酶(phosphorylated mitogen-activated protein kinase kinase,p-MEK)和磷酸化细胞外信号调节激酶1/2(phosphorylated extracellular signal-regulated kinase 1/2,p-ERK1/2)表达水平。结果表明EAT和EαA组大鼠逃避潜伏期显著低于E组;穿越平台次数显著高于E组(P<0.01)。EATC和EαAR组大鼠逃避潜伏期最短,穿越平台次数最多(P<0.01)。EATU和EαAU大鼠逃避潜伏期最长,穿越平台次数最少(P<0.01)。EAT和EαA组RGS14蛋白和mRNA表达水平显著低于E组,Raf-1、p-MEK和p-ERK1/2表达水平则显著高于E组(P<0.01)。EATC和EαAR组RGS14蛋白和mRNA表达水平最低,显著低于其他各组,Raf-1、p-MEK和p-ERK1/2表达水平最高,显著高于其他各组(P<0.01或P<0.05)。EATU和EαAU组p-MEK、p-ERK1/2表达水平最低,显著低于其他各组(P<0.01)。以上实验结果表明石菖蒲和α-细辛醚能够基于对海马RGS14/MEK/ERK信号通路的调节,从而显著提高疲劳运动大鼠的学习记忆。展开更多
基金funded by the Research and Product Development of Key Technologies for Efficient Utilization of Walnut Meal(20210203125SF)Changchun 2021 Local Transformation of Scientific and Technological Achievements Guide Special(21KY05).
文摘In study,we investigated the effect of treatment with combination of walnut peptides with molecular weight<3 kDa and ginsenoside Rg1(<3 kDa+Rg1)on scopolamine-induced cognitive impairment in mice and the mechanism of brain-derived neurotrophic factor(BDNF)/tyrosine kinase B(TrKB)/cAMP response element-binding protein(CREB)signaling pathway in PC12 cells.In behavioral experiments,<3 kDa+Rg1 treatment improved the memorizing ability of mice.Treatment with<3 kDa+Rg1 significantly regulated the function of neurotransmitters and effectively improved the morphology of the neurons determined by hematoxylin and eosin(H&E),Nissl,and Golgi staining.Additionally,immunohistochemistry showed that the<3 kDa+Rg1 treatment significantly decreased acetylcholinesterase(AChE)activity and increased choline acetyl transferase(ChAT)content in the hippocampus.The treatment upregulated vesicular acetylcholine transporter(VAChT),activated the BDNF/TrKB/CREB signaling pathway,improved the remodeling of dendritic spines,and enhanced cholinergic functions.In the scopolamine-induced PC12 cells,combination treatment increased thioredoxin-1(Trx-1)expression after administering TrKB and activated signaling pathway.The results showed combination of<3 kDa+Rg1 activated the BDNF/TrKB/CREB signaling pathway by regulating function of neurotransmitters and enhanced cholinergic function to decrease cognitive impairment.
文摘研究石菖蒲和α-细辛醚抵抗大鼠疲劳运动后学习记忆下降的RGS14/MEK/ERK信号通路作用机制。80只SD大鼠按完全随机法分为:正常组(normal,Nor)、运动组(exercise,E)、运动+石菖蒲组(exercise+Acorus tatarinowii Schott,EAT)、运动+α-细辛醚组(exercise+α-asarone,EαA)、运动+石菖蒲+RGS14拮抗剂CCG-63802组(EATC)、运动+α-细辛醚+RGS14拮抗剂CCG-63802(EαAR)、运动+石菖蒲+MEK拮抗剂U0126组(EATU)、运动+α-细辛醚+MEK拮抗剂U0126组(EαAU),每组10只。开展水迷宫实验进行学习记忆检测;利用免疫组化、免疫印迹(Western blot)和荧光实时定量PCR(RT-PCR)等方法检测G蛋白信号调节蛋白14(regulator of G protein signaling 14,RGS14)、Raf-1、磷酸化丝裂原活化蛋白激酶激酶(phosphorylated mitogen-activated protein kinase kinase,p-MEK)和磷酸化细胞外信号调节激酶1/2(phosphorylated extracellular signal-regulated kinase 1/2,p-ERK1/2)表达水平。结果表明EAT和EαA组大鼠逃避潜伏期显著低于E组;穿越平台次数显著高于E组(P<0.01)。EATC和EαAR组大鼠逃避潜伏期最短,穿越平台次数最多(P<0.01)。EATU和EαAU大鼠逃避潜伏期最长,穿越平台次数最少(P<0.01)。EAT和EαA组RGS14蛋白和mRNA表达水平显著低于E组,Raf-1、p-MEK和p-ERK1/2表达水平则显著高于E组(P<0.01)。EATC和EαAR组RGS14蛋白和mRNA表达水平最低,显著低于其他各组,Raf-1、p-MEK和p-ERK1/2表达水平最高,显著高于其他各组(P<0.01或P<0.05)。EATU和EαAU组p-MEK、p-ERK1/2表达水平最低,显著低于其他各组(P<0.01)。以上实验结果表明石菖蒲和α-细辛醚能够基于对海马RGS14/MEK/ERK信号通路的调节,从而显著提高疲劳运动大鼠的学习记忆。
