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Sodium valproate suppresses abnormal neurogenesis induced by convulsive status epilepticus

Neural Regeneration Research 2019年第3期14卷 480-484页

作者： Peng Wu Yue Hu Xiu-Juan Li Min Cheng Li Jiang department of neurology Children's Hospital of Chongqing Medical University Chongqing International Science and Technology Cooperation Center for Child Development and disorders Ministry of Education Key Laboratory of Child Development and disorders Key Laboratory of Pediatrics in Chongqing

Status epilepticus has been shown to activate the proliferation of neural stem cells in the hippocampus of the brain, while also causing a large amount of neuronal death, especially in the subgranular zone of the dentate gyrus and the subventricular zone. Simultaneously, proliferating stem cells tend to migrate to areas with obvious damage. Our previous studies have clearly confirmed the effect of sodium valproate on cognitive function in rats with convulsive status epilepticus. However, whether neurogenesis can play a role in the antiepileptic effect of sodium valproate remains unknown. A model of convulsive status epilepticus was established in Wistar rats by intraperitoneal injection of 3 mEq/kg lithium chloride, and intraperitoneal injection of pilocarpine 40 mg/kg after 18–20 hours. Sodium valproate(100, 200, 300, 400, 500, or 600 mg/kg) was intragastrically administered six times every day(4-hour intervals) for 5 days. To determine the best dosage, sodium valproate concentration was measured from the plasma. The effective concentration of sodium valproate in the plasma of the rats that received the 300-mg/kg intervention was 82.26 ± 11.23 μg/mL. Thus, 300 mg/kg was subsequently used as the intervention concentration of sodium valproate. The following changes were seen: Recording excitatory postsynaptic potentials in the CA1 region revealed high-frequency stimulation-induced long-term potentiation. Immunohistochemical staining for BrdU-positive cells in the brain revealed that sodium valproate intervention markedly increased the success rate and the duration of induced long-term potentiation in rats with convulsive status epilepticus. The intervention also reduced the number of newborn neurons in the subgranular area of the hippocampus and subventricular zone and inhibited the migration of newborn neurons to the dentate gyrus. These results indicate that sodium valproate can effectively inhibit the abnormal proliferation and migration of neural stem cells and n

关键词： nerve regeneration status epilepticus sodium valproate long-term potentiation neural stem cells neurogenesis migration subgranular zone subventricular zone neural regeneration

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Rare variant analysis of PLXNA1 in Parkinson’s disease in the Chinese population

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Genes & Diseases 2023年第4期10卷 1200-1202页

作者： Chunyu Li Ruwei Ou Yanbing Hou Junyu Lin Kuncheng Liu Qianqian Wei Xueping Chen Wei Song Bi Zhao Huifang Shang department of neurology Laboratory of Neurodegenerative DisordersNational Clinical Research Center for GeriatricsWest China HospitalSichuan UniversityChengduSichuan 610041China

Recently,***1121Ter in PLXNA1 was identified as po-tential cause for a patient with ***,no further replication has been conducted in a wider range of Parkinson’s disease(PD)*** evaluate the genetic association of PLXNA1 with PD,we systematically analyzed the rare protein-coding variants in 1,245 Chinese patients with whole exome sequencing.

关键词： PLX patients Rare

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Molecular Mediators of Estrogen Reduction-induced Otolith Shedding

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Current Medical Science 2021年第4期41卷 667-672页

作者： Mei-yan FENG Huan-huan GU Qing TIAN Hua-lan YANG Jian-hua ZHUANG department of neurology Medical Center for Vertigo and Balance DisordersShanghai Changzheng Hospital of Navy Medical UniversityShanghai200003China department of neurology Shanghai Pudong HospitalFudan University Pudong Medical CenterShanghai201399China

Objective Previous study suggested that estradiol(E2)plays an important role in otolith shedding by regulating the expression of otoconin 90(OC90).The purpose of this article is to provide further data on the effect and mechanism of E2 on the morphology of *** The rats receiving bilateral ovariectomy(OVX)were used as animal ***-immunoprecipitation was used to observe the relationship between estrogen receptor(ER)and estrogen-related receptorα(ERRα).The morphology of otolith was observed under the scanning electron *** blotting and qPCR were used for quantitative analysis of the roles of ER and ERRαin regulating OC90 *** The looser otoliths were observed in rats receiving bilateral OVX,which could be reversed by supplementation with *** level of ERRαwas decreased in bilateral OVX *** and ERRαinteracted with each other on the regulation of the expression of *** Our results suggest ER and ERRαare both important downstream receptors involved in regulating OC90 expression in utricles of rats,and ERRαprobably functions by interacting with *** provides evidence for the mechanism of otolith *** it may be significant for future studies of targeted prevention and therapies for benign paroxysmal positional vertigo.

关键词： estrogen-related receptorα estrogen receptor otoconin 90 otolith benign paroxysmal positional vertigo

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Advances in longitudinal studies of amnestic mild cognitive impairment and Alzheimer's disease based on multi-modal MRI techniques

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Neuroscience Bulletin 2014年第2期30卷 198-206页

作者： Zhongjie Hu Liyong Wu Jianping Jia Ying Han department of neurology Xuan Wu Hospital Capital Medical University Postgraduates Institute Capital Medical University Alzheimer's Disease Center Beijing Institute for Brain Disorders

Amnestic mild cognitive impairment （aMCI） is a prodromal stage of Alzheimer＇s disease （AD）, and 75%-80% of aMCI patients finally develop AD. So, early identification of patients with aMCI or AD is of great significance for prevention and intervention. According to cross-sectional studies, it is known that the hippocampus, posterior cingulate cortex, and corpus callosum are key areas in studies based on structural MRI （sMRI）, functional MRI （fMRI）, and diffusion tensor imaging （DTI） respectively. Recently, longitudinal studies using each MRI modality have demonstrated that the neuroimaging abnormalities generally involve the posterior brain regions at the very beginning and then gradually affect the anterior areas during the progression of aMCI to AD. However, it is not known whether follow-up studies based on multi-modal neuroimaging techniques （e.g., sMRI, fMRI, and DTI） can help build effective MRI models that can be directly applied to the screening and diagnosis of aMCI and AD. Thus, in the future, large-scale multi-center follow-up studies are urgently needed, not only to build an MRI diagnostic model that can be used on a single person, but also to evaluate the variability and stability of the model in the general population. In this review, we present longitudinal studies using each MRI modality separately, and then discuss the future directions in this field.

关键词： magnetic resonance imaging amnestic mild cognitive impairment Alzheimer's disease multi-modality longitudinal studies

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Regulation of adenosine triphosphate-sensitive potassium channels suppresses the toxic effects of amyloid-beta peptide(25-35)

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Neural Regeneration Research 2013年第1期8卷 56-63页

作者： Min Kong Maowen Ba Hui Liang Peng Shao Tianxia Yu Ying Wang department of neurology Yantaishan Hospital department of neurology Yuhuangding Hospital Affiliated to Qingdao Medical University

In this study, we treated PC12 cells with 0-20 μM amyloid-β peptide （25-35） for 24 hours to induce cytotoxicity, and found that 5-20 μM amyloid-β peptide （25-35） decreased PC12 cell viability, but adenosine triphosphate-sensitive potassium channel activator diazoxide suppressed the decrease in PC12 cell viability induced by amyloid-β peptide （25-35）. Diazoxide protected PC12 cells against amyloid-β peptide （25-35）-induced increases in mitochondrial membrane potential and intracellular reactive oxygen species levels. These protective effects were reversed by the selective mitochondrial adenosine triphosphate-sensitive potassium channel blocker 5-hydroxydecanoate. An inducible nitric oxide synthase inhibitor, Nw-nitro-L-arginine, also protected PC12 cells from amyloid-β peptide （25-35）-induced increases in both mitochondrial membrane potential and intracellular reactive oxygen species levels. However, the H202-degrading enzyme catalase could not reverse the amyloid-β peptide （25-35）-induced increase in intracellular reactive oxygen species. A 24-hour exposure to amyloid-13 peptide （25-35） did not result in apoptosis or necrosis, suggesting that the increases in both mitochondrial membrane potential and reactive oxygen species levels preceded cell death. The data suggest that amyloid-β peptide （25-35） cytotoxicity is associated with adenosine triphosphate-sensitive potassium channels and nitric oxide. Regulation of adenosine triphosphate-sensitive potassium channels suppresses PC12 cell cytotoxicity induced by amyloid-β peptide （25-35）.

关键词： neural regeneration neurodegenerative diseases amyloid-β peptide (25-35) PC12 cell adenosinetriphosphate-sensitive potassium channel inducible nitric oxide synthase mitochondrial membranepotential reactive oxygen species grant-supported paper photographs-containing paper neuroregeneration

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EZH2-dependent myelination following sciatic nerve injury

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Neural Regeneration Research 2025年第8期20卷 2382-2394页

作者： Hui Zhu Li Mu Xi Xu Tianyi Huang Ying Wang Siyuan Xu Yiting Wang Wencong Wang Zhiping Wang Hongkui Wang Chengbin Xue Research Center of Clinical Medicine Affiliated Hospital of Nantong UniversityKey Laboratory of Neuroregeneration of Jiangsu and Ministry of EducationCo-innovation Center of NeuroregenerationNMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology ProductsNantong UniversityNantongJiangsu ProvinceChina Medical School of Nantong University NantongJiangsu ProvinceChina department of neurology Affiliated Hospital of Nantong UniversityNantongJiangsu ProvinceChina department of Rehabilitation Medicine Affiliated Hospital of Nantong UniversityNantongJiangsu ProvinceChina department of Critical Care Medicine Nantong Fourth People’s HospitalNantongJiangsu ProvinceChina

Demyelination and remyelination have been major focal points in the study of peripheral nerve regeneration following peripheral nerve ***,the gene regulatory network of regenerated myelin differs from that of native *** of enhancer of zeste homolog 2(EZH2)hinders the differentiation,maturation,and myelination of Schwann cells in *** further determine the role of EZH2 in myelination and recovery post-peripheral nerve injury,conditional knockout mice lacking Ezh2 in Schwann cells(Ezh2^(fl/fl);Dhh-Cre and Ezh2^(fl/fl);Mpz-Cre)were *** results show that a significant proportion of axons in the sciatic nerve of Ezh2-depleted mice remain *** highlights the crucial role of Ezh2 in initiating Schwann cell ***,we observed that 21 days after inducing a sciatic nerve crush injury in these mice,most axons had remyelinated at the injury site in the control nerve,while Ezh2^(fl/fl);Mpz-Cre mice had significantly fewer remyelinated axons compared with their wild-type *** suggests that the absence of Ezh2 in Schwann cells impairs myelin formation and *** conclusion,EZH2 has emerged as a pivotal regulatory factor in the process of demyelination and myelin regeneration following peripheral nerve *** EZH2 activity during these processes may offer a promising therapeutic target for the treatment of peripheral nerve injuries.

关键词： demyelination EZH2 myelination peripheral nerve injury PRC2 remyelination Schwann cells sciatic nerve crush sciatic nerve transection

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Nerve conduction models in myelinated and unmyelinated nerves based on three-dimensional electrostatic interaction

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Neural Regeneration Research 2018年第5期13卷 779-785页

作者： Tetsuya Akaishi department of neurology Tohoku University Graduate School of Medicine department of neurology Yonezawa National Hospital

Until now, nerve conduction has been described on the basis of equivalent circuit model and cable theory, both of which supposed closed electric circuits spreading inside and outside the axoplasm. With these conventional models, we can simulate the propagating pattern of action potential along the axonal membrane based on Ohm＇s law and Kirchhoff＇s law. However, we could not fully explain the different conductive patterns in unmyelinated and myelinated nerves with these theories. Also, whether we can really suppose closed electrical circuits in the actual site of the nerves or not has not been fully discussed yet. In this report, a recently introduced new theoretical model of nerve conduction based on electrostatic molecular interactions within the axoplasm will be reviewed. With this new approach, we can explain the different conductive patterns in unmyelinated and myelinated nerves. This new mathematical conductive model based on electrostatic compressional wave in the intracellular fluid may also be able to explain the signal integration in the neuronal cell body and the back-propagation mechanism from the axons to the dendrites. With this new mathematical nerve conduction model based on electrostatic molecular interactions within the intracellular fluid, we may be able to achieve an integrated explanation for the physiological phenomena taking place in the nervous system.

关键词： nerve conduction ion channels electrostatic interactions electrostatic compressional wave saltatory conduction myelinated nerves unmyelinated nerves saltatory equations

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The pathways by which mild hypothermia inhibits neuronal apoptosis following ischemia/reperfusion injury

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Neural Regeneration Research 2015年第1期10卷 153-158页

作者： Chun Luo Su-yue Pan department of neurology Nanfang HospitalSouthern Medical University department of neurology Guangxi Minzu Hospital

Several studies have demonstrated that mild hypothermia exhibits a neuroprotective role and it can inhibit endothelial cell apoptosis following ischemia/reperfusion injury by decreasing casp- ase-3 expression, It is hypothesized that mild hypothermia exhibits neuroprotective effects on neurons exposed to ischemia/reperfusion condition produced by oxygen-glucose deprivation. Mild hypothermia significantly reduced the number of apoptotic neurons, decreased the expres- sion of pro-apoptotic protein Bax and increased mitochondrial membrane potential, with the peak of anti-apoptotic effect appearing between 6 and 12 hours after the injury. These findings indicate that mild hypothermia inhibits neuronal apoptosis following ischemia/reperfusion injury by protecting the mitochondria and that the effective time window is 6-12 hours after ischemia/reperfusion injury.

关键词： nerve regeneration mild hypothermia oxygen-glucose deprivation cell apoptosis neu-rons mitochondrial membrane potential Bax ischemia/reperfusion neural regeneration

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Deciphering the molecular mechanisms of Simiaowan in the treatment of hyperuricemia: in vivo and in silico approaches

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Traditional Medicine Research 2025年第2期10卷 37-54页

作者： Yong-Chang Zeng Jun-Hong Wu Dan-Dan Xu Kang He Chang-Qing Liu Li-Fei Song Zheng-Zhi Wu Qian-Qian Jiang Shao-Yu Liang department of neurology The First Affiliated Hospital of Shenzhen UniversityShenzhen 518020China Pharmaceutical department The Affiliated TCM Hospital of Guangzhou Medical UniversityGuangzhou 510000China School of Pharmacy Guizhou University of Traditional Chinese MedicineGuiyang 550025China Guangzhou Zeli Medical Technology Co. Ltd.Guangzhou 510700China

Background:Simiaowan(SMW),a well-known traditional Chinese medicine,has been employed to treat hyperuricemia(HUA)and gout for ***,the bioactive components and underlying mechanisms have not been *** objective of this study was to identify the active components and potential mechanisms of SMW by integrating pharmacological experimentation,serum pharmacochemistry,network pharmacology and molecular ***:HUA rats modelling by high-fat/high-sugar diet and potassium oxonate/adenine oral administration were used to evaluate the pharmacodynamic effects of ***-Q-Exactive-MS/MS was employed to detect the bioactive components present in SMW-containing *** pharmacology and molecular docking were utilized to elucidate the potential targets and underlying ***:SMW effectively ameliorated HUA rats via the inhibition of uric acid(UA)production,promotion of UA excretion,improvement of lipid and glucose metabolic abnormalities,antioxidant,anti-inflammatory and anti-insulin resistance effects.A total of 73 compounds detected in SMW-containing serum were identified as potential active components,with alkaloids,flavonoids,organic acids,and terpenoids emerging as the primary active *** 203 corresponding targets were obtained as SMW anti-HUA/gout targets,which mainly participated in apoptosis,insulin resistance,TNF,PI3K-Akt,HIF-1,NF-κB,MAPK,IL-17 and TLR signaling *** docking indicated that active compounds(***,phellodendrine,quercetin,formononetin,ferulic acid)had superior binding abilities to the key targets(*** carrier family 22 member 12(URAT1),solute carrier family 22 member 6(OAT1),ATP-binding cassette sub-family G member 2(ABCG2),solute carrier family 2,facilitated glucose transporter member 9(GLUT9),xanthine dehydrogenase/oxidase(XDH),transcription factor p65(RELA),toll-like receptor 4(TLR4),prostaglandin G/H synthase 2(PTGS2),caspase-3(CASP3),insulin(INS)).Conclusion:S

关键词： hyperuricemia network pharmacology serum pharmacochemistry Simiaowan UPLC-Q-Exactive-MS/MS

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Future needs for informed consent in stem cell clinical trials in neurodegenerative diseases

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Neural Regeneration Research 2016年第1期11卷 83-85页

作者： Natalie Hellmers Yaa Obeng-Aduasare Inmaculada de Melo-Martín Claire Henchcliffe Weill Cornell Parkinson’s Disease and Movement disorders Institute Department of Neurology Weill Cornell Medical College Division of Medical Ethics Department of Medicine Weill Cornell Medical College

Translation of recent advances in stem cell research into clinical trials for restorative therapies for human disease is accelerating dramatically,with a strong focus upon neurodegenerative disorders such as Parkinson... 详细信息

关键词： consent informed amyotrophic restorative Huntington likely advances accelerating comprehension intracerebral

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