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Copper homeostasis and neurodegenerative diseases

Neural Regeneration Research 2025年第11期20卷 3124-3143页

作者： Yuanyuan Wang Daidi Li Kaifei Xu Guoqing Wang Feng Zhang International Research laboratory of Ethnomedicine of ministry of education Key Laboratory of Basic Pharmacology of Ministry of EducationLaboratory Animal Center and Key Laboratory of Basic Pharmacology of Guizhou ProvinceZunyi Medical UniversityZunyiGuizhou ProvinceChina

Copper,one of the most prolific transition metals in the body,is required for normal brain physiological activity and allows various functions to work normally through its range of *** homeostasis is meticulously maintained through a complex network of copper-dependent proteins,including copper transporters(CTR1 and CTR2),the two copper ion transporters the Cu-transporting ATPase 1(ATP7A)and Cu-transporting beta(ATP7B),and the three copper chaperones ATOX1,CCS,and *** in copper homeostasis can lead to either the deficiency or accumulation of copper in brain *** evidence suggests that abnormal copper metabolism or copper binding to various proteins,including ceruloplasmin and metallothionein,is involved in the pathogenesis of neurodegenerative ***,the exact mechanisms underlying these processes are not *** is a potent oxidant that increases reactive oxygen species production and promotes oxidative *** reactive oxygen species levels may further compromise mitochondrial integrity and cause mitochondrial *** oxygen species serve as key signaling molecules in copper-induced neuroinflammation,with elevated levels activating several critical inflammatory ***,copper can bind aberrantly to several neuronal proteins,including alphasynuclein,tau,superoxide dismutase 1,and huntingtin,thereby inducing neurotoxicity and ultimately cell *** study focuses on the latest literature evaluating the role of copper in neurodegenerative diseases,with a particular focus on copper-containing metalloenzymes and copper-binding proteins in the regulation of copper homeostasis and their involvement in neurodegenerative disease *** synthesizing the current findings on the functions of copper in oxidative stress,neuroinflammation,mitochondrial dysfunction,and protein misfolding,we aim to elucidate the mechanisms by which copper contributes to a wide range of heredit

关键词： Alzheimer's disease amyotrophic lateral sclerosis disease copper homeostasis copper toxicity Huntington's disease Menkes'disease multiple sclerosis neurodegenerative disease Parkinson's disease Wilson's disease

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Hippocampal neurogenesis and pro-neurogenic therapies for Alzheimer's disease

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Animal Models and Experimental Medicine 2022年第1期5卷 3-14页

作者： Jie Zheng Department of pharmacology Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnomedicine of Ministry of EducationKey Laboratory of Basic Pharmacology of Guizhou ProvinceZunyi Medical UniversityZunyiChina

Adult hippocampal neurogenesis(AHN)facilitates hippocampal circuits plasticity and regulates hippocampus-dependent cognition and ***,AHN malfunction has been widely reported in both human and animal models of Alzheimer's disease(AD),the most common form of dementia in the *** therapies including rescuing innate AHN,cell engraftment and glianeuron reprogramming hold great potential for compensating the neuronal loss and rewiring the degenerated neuronal network in AD,but there are still great challenges to be *** review covers recent advances in unraveling the involvement of AHN in AD and highlights the prospect of emerging proneurogenic remedies.

关键词： Alzheimer's disease cognitive deficit hippocampus neurogenesis pro-neurogenic therapy

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Resolving the developmental mechanisms of cardiac microthrombosis of SARS-CoV-2 based on single-cell transcriptome analysis

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Science China Life Sciences 2025年第01期 103-115页

作者： Xizi Luo Nan Zhang Yuntao Liu Beibei Du Xuan Wang Tianxu Zhao Bingqiang Liu Shishun Zhao Jiazhang Qiu Guoqing Wang State key laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases Key Laboratory for Zoonosis Research of the Ministry of EducationCollege of Basic MedicineJilin University State key laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases Key Laboratory for Zoonosis Research of the Ministry of EducationCollege of Veterinary MedicineJilin University College of Mathematics Jilin University Bioinformatic lab School of MathematicsShandong University Department of Cardiology China-Japan Union HospitalJilin University

The coronavirus disease 2019（COVID-19） outbreak caused by the severe acute respiratory syndrome coronavirus-2（SARS-CoV-2） developed into a global health emergency. Systemic microthrombus caused by SARS-CoV-2 infection is a common complication in patients with COVID-19. Cardiac microthrombosis as a complication of SARS-CoV-2 infection is the primary cause of cardiac injury and death in patietns with severe COVID-19. In this study, we performed single-cell sequencing analysis of the right ventricular free wall tissue from healthy donors,patients who died during the hypercoagulable period of characteristic coagulation abnormality（CAC）, and patients who died during the fibrinolytic period of CAC. We collected 61,187 cells enriched in 24 immune cell subsets and 13 cardiac-resident cell subsets. We found that in the course of SARS-CoV-2 infected heart microthrombus, MYO1EhighRASGEF1Bhighmonocyte-derived macrophages promoted hyperactivation of the immune system and initiated the extrinsic coagulation pathway by activating chemokines CCL3, CCL5. This series of events is the main cause of cardiac microthrombi following SARS-CoV-2 infection. In a SARS-CoV-2 infected heart microthrombus, excessive immune activation is accompanied by an increase in cellular iron content, which in turn promotes oxidative stress and intensifies intercellular competition. This induces cells to alter their metabolic environment, resulting in increased sugar uptake via the glycosaminoglycan synthesis pathway. In addition, high levels of reactive oxygen species generated by elevated iron levels promote increased endogenous malondialdehyde synthesis in a subpopulation of cardiac endothelial cells. This exacerbates endothelial cell dysfunction and exacerbates the coagulopathy process.

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Potential neuroprotection by Dendrobium nobile Lindl alkaloid in Alzheimer's disease models

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Neural Regeneration Research 2022年第5期17卷 972-977页

作者： Dai-Di Li Chang-Qing Zheng Feng Zhang Jing-Shan Shi key laboratory of basic pharmacology of ministry of education and Joint International Research lab of Ethnomedicine of ministry of education Zunyi MedicalUniversityZunyiGuizhou ProvinceChina School of Pharmacy Shanghai University of Traditional Chinese MedicineShanghaiChina

At present,treatments for Alzheimer's disease can temporarily relieve symptoms but cannot prevent the decline of cognitive ability and other neurodegenerative *** nobile Lindl alkaloid is the main active component of Dendrobium nobile *** nobile Lindl alkaloid has been shown to resist aging,prolong life span,and exhibit immunomodulatory effects in *** review summarizes the mechanisms behind the neuroprotective effects reported in Alzheimer's disease animal *** neuroprotective effects of Dendrobium nobile Lindl alkaloid have not been studied in *** mechanisms by which Dendrobium nobile Lindl alkaloid has been reported to improve cognitive dysfunction in Alzheimer's disease animal models may be associated with extracellular amyloid plaque production,regulation of tau protein hyperphosphorylation,inhibition of neuroinflammation and neuronal apoptosis,activation of autophagy,and enhanced synaptic connections.

关键词： Alzheimer's disease amyloidβplaques animal models Dendrobium

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Protective effects of Dendrobium nobile Lindl. alkaloids on amyloid beta(25–35)-induced neuronal injury

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Neural Regeneration Research 2017年第7期12卷 1131-1136页

作者： Wei Zhang Qin Wu Yan-liu Lu Qi-hai Gong Feng Zhang Jing-shan Shi key laboratory of basic pharmacology of ministry of education and Joint International Research laboratory of Ethnomedicine of ministry ofeducation Zunyi Medical University Zunyi Guizhou Province China

Dendrobium nobile ***（DNLA）,the active ingredients of a traditional Chinese medicine Dendrobium,have been shown to have anti-oxidative effects,anti-inflammatory action,and protective effect on neurons against oxygen-glucose ***,it is not clear whether DNLA reduces amyloid-beta（Aβ）-induced neuronal *** this study,cortical neurons were treated with DNLA at different concentrations（0.025,0.25,and 2.5 mg/L）for 24 hours,followed by administration of Aβ（25-35）（10μM）.Aβ（25-35） treatments increased cell injury as determined by the leakage of lactate dehydrogenase,which was accompanied by chromatin condensation and mitochondrial *** damage caused by Aβ（25-35） on these cellular properties was markedly attenuated when cells were pretreated with *** with Aβ（25-35）down-regulated the expressions of postsynaptic density-95 mRNA and decreased the protein expression of synaptophysin and postsynaptic density-95,all changes were significantly reduced by pretreatment of cells with *** findings suggest that DNLA reduces the cytotoxicity induced by Aβ（25-35） in rat primary cultured *** protective mechanism that DNLA confers on the synaptic integrity of cultured neurons might be mediated,at least in part,through the upregulation of neurogenesis related proteins synaptophysin and postsynaptic density-95.

关键词： nerve regeneration Dendrobium nobile Lindl. alkaloids amyloid beta neurons synapse synaptophysin postsynaptic density-95 cognitive impairment neuroprotection neural regeneration

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A novel dephosphorylation targeting chimera selectively promoting tau removal in tauopathies

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Signal Transduction and Targeted Therapy 2021年第8期6卷 2511-2520页

作者： Jie Zheng Na Tian Fei Liu Yidian Zhang Jingfen Su Yang Gao Mingmin Deng Linyu Wei Jingwang Ye Honglian Li Jian-Zhi Wang Department of Pathophysiology School of Basic MedicineKey Laboratory of Education Ministry of China/Hubei Province for Neurological DisordersTongji Medical CollegeHuazhong University of Science and TechnologyWuhanChina Department of pharmacology Key Laboratory of Basic Pharmacology of Ministry of EducationJoint International Research Laboratory of Ethnomedicine of Ministry of EducationKey Laboratory of Basic Pharmacology of Guizhou ProvinceZunyi Medical UniversityZunyiChina Department of Histology and Embryology Key Laboratory of Ministry of Education for Neurological DisordersSchool of Basic MedicineTongji Medical CollegeHuazhong University of Science and TechnologyWuhanChina Co-innovation Center of Neuroregeneration Nantong UniversityNantongChina

Intraneuronal accumulation of hyperphosphorylated tau is a hallmark pathology shown in over twenty neurodegenerative disorders,collectively termed as tauopathies,including the most common Alzheimer's disease(AD).Therefore,selectively removing or reducing hyperphosphorylated tau is promising for therapies of AD and other ***,we designed and synthesized a novel DEPhosphorylation TArgeting Chimera(DEPTAC)to specifically facilitate the binding of tau to Ba-subunit-contalning protein phosphatase 2A(PP2A-Ba),the most active tau phosphatase in the *** DEPTAC exhibited high efficiency in dephosphorylating tau at multiple AD-associated sites and preventing tau accumulation both in vitro and in *** studies revealed that DEPTAC significantly improved microtubule assembly,neurite plasticity,and hippocampus-dependent learning and memory in transgenic mice with inducible overexpression of truncated and neurotoxic human tau *** data provide a strategy for selective removal of the hyperphosphorylated tau,which sheds new light for the targeted therapy of AD and related-tauopathies.

关键词： tau Alzheimer removing

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Heat-killed Lactobacillus murinus confers neuroprotection against dopamine neuronal loss by targeting NLRP3 inflammasome

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中国药理学与毒理学杂志 2023年第7期37卷 521-522页

作者： LI Daidi FAN Hongxia ZHANG Feng key laboratory of basic pharmacology of ministry of education and Joint International Research laboratory of Ethnomedicine of ministry of education and key laboratory of basic pharmacology of Guizhou Province Zunyi Medical University

OBJECTIVE In this study, the effects of live Lactobacillus murinus(L. m) and heat-killed ***(H-k L. m) on DA neuronal damage in rats and the underlying mechanisms were investigated. METHODS Male SD rats were randomly divided into five groups:vehicle group, L. m/H-k L. m(1×109cfu) group, 6-OHDH group, 6-OHDH + L. m/H-k L. m(1×107cfu) group, and 6-OHDH + L. m/H-k L. m(1×109cfu) group. Wild-type and NLRP3 knockout mice were divided into three groups:sham(vehicle), 6-OHDH, and 6-OHDH + H-k L. m(1×109cfu). The model was established after five weeks of preadministration. Motor ability of experimental mice was assessed by rotarod, mine, and stepping experiments;the expression of dopaminergic neuron markers — tyrosine hydroxylase(TH), microglial cell markers—ionized calnexin 1(IBA-1), and NOD-like receptor family protein3(NLRP3) in the substantia nigra was detected by immunohistochemistry and immunofluorescence experiments. The expression changes of TH, IBA-1, NLRP3,apoptosis-associated microparticle protein(ASC), caspase 1, and inflammatory factors such as interleukin-1β(IL-1β), IL-18, and tumor necrosis factor-α(TNF-α) were detected by immunoblotting experiments. RESULTS H-k L. m ameliorated 6-OHDH-induced motor dysfunctions and loss of substantia nigra DA neurons, while no protection was shown in live L.m treatment. At the same time,H-k L. m reduced the activation of NLRP3 inflammasome in microglia and the secretion of pro-inflammatory factors,thus inhibiting the development of neuroinflammation. Furthermore, H-k L. m failed to display its original neuroprotective properties in NLRP3 inflammasome knockout mice. CONCLUSION H-k L. m conferred neuroprotection against DA neuronal loss via the inhibition of microglial NLRP3 inflammasome activation, these findings provide a promising potential for future applications of L. m, and also beneficial strategy for PD treatment.

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Microstructural evolution of ECAPed 1050 alloy under magnetic annealing

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International Journal of Minerals,Metallurgy and Materials 2014年第12期21卷 1205-1214页

作者： Yi-heng Cao Pin-feng Jia Kang Wang Li-zi He Ping Wang Jian-zhong Cui key lab of Electromagnetic Processing of Materials Ministry of Education Northeastern University

Hardness and microstructure evolutions in 1050 aluminum alloy prepared by equal-channel angular pressing （ECAP） were inves- tigated by hardness testing, optical microscopy, and transmission electron microscopy after samples were annealed at different temperatures for 1 h both in the absence and presence of a 12-T magnetic field. The results showed that the hardness of samples after magnetic annealing were lower than that of samples after normal annealing at 150-250℃, but it was higher than that of samples after normal annealing at 〉250℃. During annealing, the rate of softening was faster, and the grains were more homogeneous in 8-ECAPed samples than in 2-ECAPed samples. A rapid grain growth occurred when 2-ECAPed samples were annealed at high temperature （〉300℃）. The magnetic field enhanced the mobility of dislocations and grain boundaries. A more homogeneous grain size was observed in samples prepared under an applied magnetic field.

关键词： aluminum alloys magnetic annealing equal channel angular pressing microstructural evolution grain growth

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Effect of icariin on ubiquitination of amyloid precursor protein in Alzheimer′s disease mice

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中国药理学与毒理学杂志 2023年第7期37卷 519-520页

作者： HE Chengfen LIN Cong CHEN Xia GONG Qihai LI Fei Department of pharmacology Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnomedicine of Ministry of Education Key Laboratory of Basic Pharmacology of Guizhou Province School of Pharmacy Zunyi Medical University

OBJECTIVE To investigate the effect of icariin (ICA) on the ubiquitination modification of β-amyloid precursor protein (APP) in Alzheimer′s disease *** In vitro,(1) HEK 293 cells stably overexpressing human APP695 (OE-h APP) were treated with different concentrations of ICA (10-100μmol·L-1) for 24 h and the cell viability was detected by MTT assay.(2) CHX(50 mg·L-1) was used to block protein synthesis and MG132 (20μmol·L-1) inhibits proteasome activity, then the level of APP in different time (0, 0.5, 1, 2, 3 and 4 h) and the ubiquitination were tested by Western blotting.(3) E3ubiquitin ligases HMG-Co A reductase degradation protein 1 (HRD1) protein expression in OE-h APP was tested by Western blotting, as well as the level and ubiquitination of APP were tested under HRD1 silent condition by Co-IP and Western blotting. In vivo,(1) male APP/PS1 mice and wild type (WT) mice were randomly divided into 5groups:WT, WT+ICA, APP/PS1, APP/PS1+ICA, and APP/PS1+donepezil (DPZ) groups. ICA (60 mg·kg-1·d-1)and DPZ (1 mg·kg-1·d-1) were treated for 3 months by gavage from 6 months of age, and WT mice were given equal volume of distilled water.(2) Morris water maze and Y-maze experiments were used to detect the alteration of spatial learning memory function.(3) After then, the brain tissues were collected, total proteins were extracted,APP antibodies were subjected to Co-IP, and total ubiquitination (Ub), K48-linked polyubiquitination (Ub K48) and K63-linked polyubiquitination of APP level, APP and HRD1 proteins were detected by Western *** In vitro results showed that ICA significantly enhanced APP degradation (vs control, P<0.01), up-regulated HRD1 expression (vs control, P <0.05; vs OE-h APP, P<0.05), elevated the level Ub and Ub K48 of APP, as well as increased APP degradation. Moreover,silenced HRD1 gene abolished abovementioned effects of ICA (vs control-si RNA, P<0.05; vs HRD1-si RNA, P<0.05). In vivo results showed that ICA improved the spatial learn

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Liver expression of Nrf2-related genes in different liver diseases

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Hepatobiliary & Pancreatic Diseases International 2015年第5期14卷 485-491页

作者： Ming-Liang Cheng Yuan-Fu Lu Hong Chen Zhong-Yang Shen Jie Liu The Affiliated Hospital of Guizhou Medical University key lab for basic pharmacology of ministry of education Zunyi Medical College The Institute of Organ Transplantation The General Hospital of Chinese People's Armed Police Forces

BACKGROUND： The KEAP1-Nrf2 antioxidant signaling pathway is important in protecting liver from various insults. However,little is known about the expression of Nrf2-related genes in human liver in different ***： This study utilized normal donor liver tissues（n=35）, samples from patients with hepatocellular carcinoma（HCC, n=24）, HBV-related cirrhosis（n=27）, alcoholic cirrhosis（n=5） and end-stage liver disease（n=13）. All of the liver tissues were from the Oriental Liver Transplant Center, Beijing,China. The expressions of Nrf2 and Nrf2-related genes, including its negative regulator Kelch-like ECH-associated protein 1（KEAP1）, its targeted gene NAD（P）H-quinone oxidoreductase 1（NQO1）, glutamate-cysteine ligase catalytic subunit（GCLC） and modified subunit（GCLM）, heme oxygenase 1（HO-1） and peroxiredoxin-1（PRDX1） were evaluated. RESULTS： The expression of Nrf2 was decreased in HCC, increased in alcoholic cirrhosis and end-stage liver disease. The expression of KEAP1 was increased in all of the liver *** most notable finding was the increased expression of NQO1 in HCC（18-fold）, alcoholic cirrhosis（6-fold）, endstage liver disease（5-fold） and HBV-related cirrhosis（3-fold）.Peri-HCC also had 4-fold higher NQO1 m RNA as compared to the normal livers. GCLC m RNA levels were lower only in HCC, as compared to the normal livers and peri-HCC *** m RNA levels were higher in HBV-related cirrhosis and end-stage liver disease. HO-1 m RNA levels were increased in all liver tissues except for HCC. Peri-HCC had higher PRDX1 m RNA levels compared with HCC and normal ***： Nrf2 and Nrf2-related genes are aberrantly expressed in the liver in different diseases and the increase of NQO1 was the most notable finding, especially in HCC.

关键词： Nrf2-related gene expression cirrhosis hepatocellular carcinoma end-stage liver disease

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