Patients with mild cognitive impairment after a transient ischemic attack were included in this study. They were treated with Yizhi Xingnao prescription, ergoloid mesylates or aspirin for 60 days. Evaluation using the...Patients with mild cognitive impairment after a transient ischemic attack were included in this study. They were treated with Yizhi Xingnao prescription, ergoloid mesylates or aspirin for 60 days. Evaluation using the Montreal Cognitive Assessment Scale showed that cognitive function was significantly improved in all patients, especially after the combined treatment of Yizhi Xingnao and aspirin. The scores from the Montreal Cognitive Assessment Scale were improved overall and the effective treatment rate was as high as 79%, which was higher than patients treated with a combination of ergoloid mesylates and aspirin, or aspirin alone. Our experimental findings indicate that YizhiXingnao prescription can improve mild cognitive impairment after a transient ischemic attack, and that it is more effective than ergoloid mesylates.展开更多
Objective:Alzheimer’s disease(AD)is along with cognitive decline due to amyloid-β(Aβ)plaques,tau hyperphospho rylation,and neuron loss.Shenqi Xingnao Granules(SQXN),a traditional Chinese medicine,significantly amel...Objective:Alzheimer’s disease(AD)is along with cognitive decline due to amyloid-β(Aβ)plaques,tau hyperphospho rylation,and neuron loss.Shenqi Xingnao Granules(SQXN),a traditional Chinese medicine,significantly ameliorated the cognitive function and daily living abilities of patients with AD.However,till date,no study has investigated the mechanism of action of SQXN on AD.The present study aimed to verify the effects of SQXN treatment on cognitive impairments and AD-like pathologies in APP/PS1 mice.Methods:Four-month-old APP/PS1 transgenic(Tg)mice were randomly divided into a model group and SQXN-treated(3.5,7,14 g/kg per day)groups.Learning-memory abilities were determined by Morris water maze and object recognition test.All mice were sacrificed and the brain samples were collected after 75 d.The soluble Aβcontents were detected by Elisa kit;The levels of expression of NeuN,APP,phosphorylated tau and related protein were measured by Western blotting;The inflammation factors were detected by the proinflammatory panel kit.Results:Four-month-old APP/PS1 mice were administered SQXN by oral gavage for 2.5 months.Using the Morris water maze tests and Novel object recognition,we found that SQXN restored behavioral deficits in the experimental group of Tg mice when compared with the controls.SQXN also inhibited neuronal loss(NeuN marker).SQXN treatment decreased soluble Aβ42 through inhibiting the expression of sAPPβand BACE-1 without regulating full-length amyloid precursor protein(FL APP).Insulin degrading enzyme(IDE),the Aβdegrading enzyme,were increased by SQXN.In addition,SQXN reduced hyperphosphorylated tau protein levels and prevented excessive activation of p-GSK-3βin the brain of APP/PS1 mice.Compared with APP/PS1 transgenic negative mice,IFN-γ,IL-1β,IL-2,IL-4,IL-5,IL-6,IL-12 p70,KC/GRO and TNF-αwere not obviously changed in the brain of 6.5-month-old APP/PS1 transgenic(Tg)mice.However,SQXN could inhibited the expression of IL-2.Conclusion:These results demonstrate that SQXN ameliorates the cognitive impairments in APP/PS1 mice.The possible mechanisms involve its inhibition of neuronal loss,soluble Aβdeposition,tau hyperphosphorylation and inflammation.展开更多
基金sponsored by Jiangsu Provincial Administration of Traditional Chinese Medicine, No. LB09090
文摘Patients with mild cognitive impairment after a transient ischemic attack were included in this study. They were treated with Yizhi Xingnao prescription, ergoloid mesylates or aspirin for 60 days. Evaluation using the Montreal Cognitive Assessment Scale showed that cognitive function was significantly improved in all patients, especially after the combined treatment of Yizhi Xingnao and aspirin. The scores from the Montreal Cognitive Assessment Scale were improved overall and the effective treatment rate was as high as 79%, which was higher than patients treated with a combination of ergoloid mesylates and aspirin, or aspirin alone. Our experimental findings indicate that YizhiXingnao prescription can improve mild cognitive impairment after a transient ischemic attack, and that it is more effective than ergoloid mesylates.
基金supported by the State Key Program of National Natural Science of China(grant number 81430100)Beijing Hundred,Thousand and Ten Thousand Talent Project(grant number 2018A04)+1 种基金National Science Fund for Distinguished Young Scholars(grant number 81625025)Beijing Municipal Science&Technology Commission(grant number Z161100000216135)。
文摘Objective:Alzheimer’s disease(AD)is along with cognitive decline due to amyloid-β(Aβ)plaques,tau hyperphospho rylation,and neuron loss.Shenqi Xingnao Granules(SQXN),a traditional Chinese medicine,significantly ameliorated the cognitive function and daily living abilities of patients with AD.However,till date,no study has investigated the mechanism of action of SQXN on AD.The present study aimed to verify the effects of SQXN treatment on cognitive impairments and AD-like pathologies in APP/PS1 mice.Methods:Four-month-old APP/PS1 transgenic(Tg)mice were randomly divided into a model group and SQXN-treated(3.5,7,14 g/kg per day)groups.Learning-memory abilities were determined by Morris water maze and object recognition test.All mice were sacrificed and the brain samples were collected after 75 d.The soluble Aβcontents were detected by Elisa kit;The levels of expression of NeuN,APP,phosphorylated tau and related protein were measured by Western blotting;The inflammation factors were detected by the proinflammatory panel kit.Results:Four-month-old APP/PS1 mice were administered SQXN by oral gavage for 2.5 months.Using the Morris water maze tests and Novel object recognition,we found that SQXN restored behavioral deficits in the experimental group of Tg mice when compared with the controls.SQXN also inhibited neuronal loss(NeuN marker).SQXN treatment decreased soluble Aβ42 through inhibiting the expression of sAPPβand BACE-1 without regulating full-length amyloid precursor protein(FL APP).Insulin degrading enzyme(IDE),the Aβdegrading enzyme,were increased by SQXN.In addition,SQXN reduced hyperphosphorylated tau protein levels and prevented excessive activation of p-GSK-3βin the brain of APP/PS1 mice.Compared with APP/PS1 transgenic negative mice,IFN-γ,IL-1β,IL-2,IL-4,IL-5,IL-6,IL-12 p70,KC/GRO and TNF-αwere not obviously changed in the brain of 6.5-month-old APP/PS1 transgenic(Tg)mice.However,SQXN could inhibited the expression of IL-2.Conclusion:These results demonstrate that SQXN ameliorates the cognitive impairments in APP/PS1 mice.The possible mechanisms involve its inhibition of neuronal loss,soluble Aβdeposition,tau hyperphosphorylation and inflammation.
