Objective:To investigate the regulatory role of cyclic adenosine monophosphate responsive element binding protein(CREB)/brain-derived neurotrophic factor(BDNF)signaling pathway in acute sleep deprivation(SD)-induced a...Objective:To investigate the regulatory role of cyclic adenosine monophosphate responsive element binding protein(CREB)/brain-derived neurotrophic factor(BDNF)signaling pathway in acute sleep deprivation(SD)-induced anxiety-like behavior mice(SD group)to study the mechanism of anxiety-like behavior better.Methods:The SD chamber was used to deprive the mice of sleep,and the anxiety-like behavior of the mice was verified using an open field test(OFT),elevated plus maze(EPM),forced swim test(FST),and tail suspension test(TST).Finally,proteins were detected by Western blotting.Result:OFT showed that the active distance and the time of stay in the central area were significantly reduced(P<0.05).EPM showed that the time and number of open arms in the SD group were significantly lower than in the control group(P<0.05).The FST showed that the forced swimming immobility time of the SD group was significantly lower than that of the control(P<0.05).Moreover,the TST showed that the immobility time of the tail suspension experiment in the SD group was significantly higher than that in the control group(P<0.05).Conclusion:Acute SD can regulate anxiety-like behavior in mice through the CREB/BDNF signaling pathway.展开更多
[Objectives] To investigate the effects of ginseng protein on gut microbiota and BDNF/TrkB signaling pathway in Alzheimer s disease (AD) mice. [Methods] D-galactose/AlCl 3 co-induction was used to establish AD model, ...[Objectives] To investigate the effects of ginseng protein on gut microbiota and BDNF/TrkB signaling pathway in Alzheimer s disease (AD) mice. [Methods] D-galactose/AlCl 3 co-induction was used to establish AD model, and mice were randomly divided into normal group 1, normal group 2, model group 1, model group 2, ginseng protein group, and microbiota transplantation group. Morris water maze experiment was used to evaluate learning and memory ability, and Western blot method was used to detect the expression of APP, p-Tau, BDNF, TrkB, p-TrkB proteins in brain tissue, and 16S rDNA was used to detect diversity of fecal microbiota. [Results] Ginseng protein and microbiota transplantation can shorten the escape latency of mice ( P <0.05), increase the number of crossing platforms ( P <0.05), reduce the expression of APP and p-Tau proteins in brain tissue ( P <0.05, P <0.01), increase the expression of BDNF, p-TrkB, p-TrkB/TrkB proteins ( P <0.05, P <0.01), and reduce the abundance of Alloprevotella, Ruminococcaceae _UCG-014, Prevotellaceae _UCG-001, and Ruminococcus _1 ( P <0.05, P <0.01). [Conclusions] The action mechanism of ginseng protein anti AD may be through regulating gut microbiota diversity and activating the BDNF/TrkB signaling pathway.展开更多
This study was to determine the protective effect of ω-3 polyunsaturated fatty acids（ω-3PUFAs） on MK-801-induced cognitive impairment in schizophrenia（SZ） rats and the underlying mechanism. A rat model of schizo...This study was to determine the protective effect of ω-3 polyunsaturated fatty acids（ω-3PUFAs） on MK-801-induced cognitive impairment in schizophrenia（SZ） rats and the underlying mechanism. A rat model of schizophrenia was induced by MK-801. The cognitive function of rats was assessed using a Morris water maze. The number of hippocampal neurons was measured by Nissl staining. The expression of CREB, p-CREB, BDNF, TrkB, p-TrkB, AKT, p-AKT, ERK, and p-ERK in the hippocampus of rats was detected by Western blotting. The results showed that ω-3PUFAs attenuated MK-801-induced cognitive impairment and hippocampal neurons loss, reversed the injury of the CREB/BDNF/TrkB pathway induced by MK-801, and antagonized MK-801-induced down-regulation of p-AKT and p-ERK in the hippocampus of rats. In conclusion, ω-3PUFAs enhances the CREB/BDNF/TrkB pathway by activating ERK and AKT, thereby increasing the synaptic plasticity and decreasing neuron loss, and antagonizing MK-801-induced cognitive impairment in schizophrenic rats.展开更多
Objective:To observe the effect of Anshen Dingzhi Decoction on tau phosphorylation in hippocampus of Alzheimer's disease rat model and its related mechanism.Methods:SD rats were randomly divided into control group...Objective:To observe the effect of Anshen Dingzhi Decoction on tau phosphorylation in hippocampus of Alzheimer's disease rat model and its related mechanism.Methods:SD rats were randomly divided into control group,model group,Anshen Dingzhi Decoction(low,medium and high dose group)and Dopazide group.Except for the control group,the rats in the other groups were injected with streptozotocin into the lateral ventricle to replicate the model of Alzheimer's disease and then given corresponding drugs for 2 weeks.orris water maze test was used to detect learning and memory ability of rats,HE staining was used to detect hippocampal histological morphology,Western-blot was used to detect tau phosphorylation level and expression abundance of BDNF and TrkB protein in hippocampal tissue of rats.Results:The escape latency of the model group was significantly increased,the number of crossing platforms and effective residence time were significantly reduced,the phosphorylation level of tau protein was significantly increased,and the phosphorylation levels of BDNF and TrkB protein were significantly decreased when compared with the control group,the difference has statistically significant(P<0.05).Anshen Dingzhi Fang could significantly reduce the escape latency of AD rats,increase the number of crossing platforms and effective residence time,inhibit the phosphorylation of tau protein,and up-regulate the phosphorylation of BDNF and TrkB protein,the difference was statistically significant when compared with the model group(P<0.05).Conclusion:Anshen Dingzhi Fang can inhibit the phosphorylation of tau protein by activating BDNF/TrkB signaling pathway and promote the learning and memory ability of AD rats.展开更多
目的:探讨金郁欢汤对抑郁状态-痰瘀互结小鼠的作用机制及BDNF/TrkB/CREB信号的影响。方法:选择成年雄性C57BL/6J小鼠30只,根据随机数字表法分为空白组、模型组、氟西汀组、低、中、高剂量金郁欢汤组,每组5只,除空白组外其余组建立抑郁状...目的:探讨金郁欢汤对抑郁状态-痰瘀互结小鼠的作用机制及BDNF/TrkB/CREB信号的影响。方法:选择成年雄性C57BL/6J小鼠30只,根据随机数字表法分为空白组、模型组、氟西汀组、低、中、高剂量金郁欢汤组,每组5只,除空白组外其余组建立抑郁状态-痰瘀互结小鼠模型。造模完成后,氟西汀组灌胃给予3 mg/kg氟西汀悬浮灌胃,金郁欢汤低、中、高剂量组分别给予0.2 g/kg、0.5 g/kg、0.8 g/kg金郁欢汤灌胃,对照组、模型组均给予等体积的生理盐水灌胃,1次/d,连续灌胃3周。对比6组小鼠造模前、造模后、给药后的体质量、糖水偏嗜率、水平得分、垂直得分、实验不动时间、实验漂浮时间、海马组织中的BDNF/TrkB/CREB m RNA及蛋白表达水平。结果:造模后,空白组的体质量、糖水偏嗜率、水平得分、垂直得分、海马组织中的BDNF/TrkB/CREB m RNA及蛋白表达水平明显较其余5组低,实验不动、漂浮时间较其余5组高(P均<0.05)。给药后,空白组、氟西汀组、中、高剂量金郁欢汤组体质量、糖水偏嗜率明显较模型组、低剂量组高,低剂量组体质量明显较模型组高(P均<0.05);空白组的水平、垂直得分明显较其余5组高,氟西汀组、中、高剂量金郁欢汤组以上指标明显较模型组、低剂量组高,低剂量组明显较模型组高(P均<0.05);空白组的实验不动、漂浮时间明显较其余5组低,氟西汀组、中、高剂量金郁欢汤组实验不动、漂浮时间显较模型组、低剂量组低,低剂量组明显较模型组低(P均<0.05);BDNF/TrkB m RNA水平、BDNF、TrkB蛋白表达水平:氟西汀组>高剂量组>中剂量组>低剂量组>空白组>模型组;其中氟西汀组、高剂量组、中剂量组三组间无差异(P>0.05),其余组间均有差异(P<0.05);CREB m RNA水平、BDNF蛋白表达:空白组>氟西汀组>高剂量组>中剂量组>低剂量组>模型组;其中空白组、氟西汀组、高剂量组、中剂量组四组间无差异(P>0.05),其余组间均有差异(P<0.05)。结论:0.5 g/kg金郁欢汤可明显改善抑郁状态-痰瘀互结小鼠的抑郁行为,增强海马神经元的修复、再生,可能与其可上调小鼠海马组织的BDNF/TrkB/CREB信号通路相关。展开更多
文摘Objective:To investigate the regulatory role of cyclic adenosine monophosphate responsive element binding protein(CREB)/brain-derived neurotrophic factor(BDNF)signaling pathway in acute sleep deprivation(SD)-induced anxiety-like behavior mice(SD group)to study the mechanism of anxiety-like behavior better.Methods:The SD chamber was used to deprive the mice of sleep,and the anxiety-like behavior of the mice was verified using an open field test(OFT),elevated plus maze(EPM),forced swim test(FST),and tail suspension test(TST).Finally,proteins were detected by Western blotting.Result:OFT showed that the active distance and the time of stay in the central area were significantly reduced(P<0.05).EPM showed that the time and number of open arms in the SD group were significantly lower than in the control group(P<0.05).The FST showed that the forced swimming immobility time of the SD group was significantly lower than that of the control(P<0.05).Moreover,the TST showed that the immobility time of the tail suspension experiment in the SD group was significantly higher than that in the control group(P<0.05).Conclusion:Acute SD can regulate anxiety-like behavior in mice through the CREB/BDNF signaling pathway.
基金Supported by Liaoning Province Science and Technology Department Project(20180530033,2022-MS-281)Liaoning Provincial Department of Education Project(LJKZZ20220105)Liaoning University of Traditional Chinese Medicine Project(2021LZY042).
文摘[Objectives] To investigate the effects of ginseng protein on gut microbiota and BDNF/TrkB signaling pathway in Alzheimer s disease (AD) mice. [Methods] D-galactose/AlCl 3 co-induction was used to establish AD model, and mice were randomly divided into normal group 1, normal group 2, model group 1, model group 2, ginseng protein group, and microbiota transplantation group. Morris water maze experiment was used to evaluate learning and memory ability, and Western blot method was used to detect the expression of APP, p-Tau, BDNF, TrkB, p-TrkB proteins in brain tissue, and 16S rDNA was used to detect diversity of fecal microbiota. [Results] Ginseng protein and microbiota transplantation can shorten the escape latency of mice ( P <0.05), increase the number of crossing platforms ( P <0.05), reduce the expression of APP and p-Tau proteins in brain tissue ( P <0.05, P <0.01), increase the expression of BDNF, p-TrkB, p-TrkB/TrkB proteins ( P <0.05, P <0.01), and reduce the abundance of Alloprevotella, Ruminococcaceae _UCG-014, Prevotellaceae _UCG-001, and Ruminococcus _1 ( P <0.05, P <0.01). [Conclusions] The action mechanism of ginseng protein anti AD may be through regulating gut microbiota diversity and activating the BDNF/TrkB signaling pathway.
基金supported in parts by grants from the Hubei Province Key Technology R&D Program(No.2015BCE094)Wuhan Science and Technology Bureau Dawn Plan Project(No.201507040410216)+1 种基金Clinical Research Physician Program of Tongji Medical CollegeHUST and the Academic Frontier Youth Team Project of HUST
文摘This study was to determine the protective effect of ω-3 polyunsaturated fatty acids（ω-3PUFAs） on MK-801-induced cognitive impairment in schizophrenia（SZ） rats and the underlying mechanism. A rat model of schizophrenia was induced by MK-801. The cognitive function of rats was assessed using a Morris water maze. The number of hippocampal neurons was measured by Nissl staining. The expression of CREB, p-CREB, BDNF, TrkB, p-TrkB, AKT, p-AKT, ERK, and p-ERK in the hippocampus of rats was detected by Western blotting. The results showed that ω-3PUFAs attenuated MK-801-induced cognitive impairment and hippocampal neurons loss, reversed the injury of the CREB/BDNF/TrkB pathway induced by MK-801, and antagonized MK-801-induced down-regulation of p-AKT and p-ERK in the hippocampus of rats. In conclusion, ω-3PUFAs enhances the CREB/BDNF/TrkB pathway by activating ERK and AKT, thereby increasing the synaptic plasticity and decreasing neuron loss, and antagonizing MK-801-induced cognitive impairment in schizophrenic rats.
基金Natural science fund of Heilongjiang province(No.H2018063).
文摘Objective:To observe the effect of Anshen Dingzhi Decoction on tau phosphorylation in hippocampus of Alzheimer's disease rat model and its related mechanism.Methods:SD rats were randomly divided into control group,model group,Anshen Dingzhi Decoction(low,medium and high dose group)and Dopazide group.Except for the control group,the rats in the other groups were injected with streptozotocin into the lateral ventricle to replicate the model of Alzheimer's disease and then given corresponding drugs for 2 weeks.orris water maze test was used to detect learning and memory ability of rats,HE staining was used to detect hippocampal histological morphology,Western-blot was used to detect tau phosphorylation level and expression abundance of BDNF and TrkB protein in hippocampal tissue of rats.Results:The escape latency of the model group was significantly increased,the number of crossing platforms and effective residence time were significantly reduced,the phosphorylation level of tau protein was significantly increased,and the phosphorylation levels of BDNF and TrkB protein were significantly decreased when compared with the control group,the difference has statistically significant(P<0.05).Anshen Dingzhi Fang could significantly reduce the escape latency of AD rats,increase the number of crossing platforms and effective residence time,inhibit the phosphorylation of tau protein,and up-regulate the phosphorylation of BDNF and TrkB protein,the difference was statistically significant when compared with the model group(P<0.05).Conclusion:Anshen Dingzhi Fang can inhibit the phosphorylation of tau protein by activating BDNF/TrkB signaling pathway and promote the learning and memory ability of AD rats.
文摘目的:探讨金郁欢汤对抑郁状态-痰瘀互结小鼠的作用机制及BDNF/TrkB/CREB信号的影响。方法:选择成年雄性C57BL/6J小鼠30只,根据随机数字表法分为空白组、模型组、氟西汀组、低、中、高剂量金郁欢汤组,每组5只,除空白组外其余组建立抑郁状态-痰瘀互结小鼠模型。造模完成后,氟西汀组灌胃给予3 mg/kg氟西汀悬浮灌胃,金郁欢汤低、中、高剂量组分别给予0.2 g/kg、0.5 g/kg、0.8 g/kg金郁欢汤灌胃,对照组、模型组均给予等体积的生理盐水灌胃,1次/d,连续灌胃3周。对比6组小鼠造模前、造模后、给药后的体质量、糖水偏嗜率、水平得分、垂直得分、实验不动时间、实验漂浮时间、海马组织中的BDNF/TrkB/CREB m RNA及蛋白表达水平。结果:造模后,空白组的体质量、糖水偏嗜率、水平得分、垂直得分、海马组织中的BDNF/TrkB/CREB m RNA及蛋白表达水平明显较其余5组低,实验不动、漂浮时间较其余5组高(P均<0.05)。给药后,空白组、氟西汀组、中、高剂量金郁欢汤组体质量、糖水偏嗜率明显较模型组、低剂量组高,低剂量组体质量明显较模型组高(P均<0.05);空白组的水平、垂直得分明显较其余5组高,氟西汀组、中、高剂量金郁欢汤组以上指标明显较模型组、低剂量组高,低剂量组明显较模型组高(P均<0.05);空白组的实验不动、漂浮时间明显较其余5组低,氟西汀组、中、高剂量金郁欢汤组实验不动、漂浮时间显较模型组、低剂量组低,低剂量组明显较模型组低(P均<0.05);BDNF/TrkB m RNA水平、BDNF、TrkB蛋白表达水平:氟西汀组>高剂量组>中剂量组>低剂量组>空白组>模型组;其中氟西汀组、高剂量组、中剂量组三组间无差异(P>0.05),其余组间均有差异(P<0.05);CREB m RNA水平、BDNF蛋白表达:空白组>氟西汀组>高剂量组>中剂量组>低剂量组>模型组;其中空白组、氟西汀组、高剂量组、中剂量组四组间无差异(P>0.05),其余组间均有差异(P<0.05)。结论:0.5 g/kg金郁欢汤可明显改善抑郁状态-痰瘀互结小鼠的抑郁行为,增强海马神经元的修复、再生,可能与其可上调小鼠海马组织的BDNF/TrkB/CREB信号通路相关。
