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General anesthetic agents induce neurotoxicity through oligodendrocytes in the developing brain

Zoological Research 2024年第3期45卷 691-703页

作者： Wen-Xin Hang Yan-Chang Yang Yu-Han Hu Fu-Quan Fang Lang Wang Xing-Hua Qian Patrick M.McQuillan Hui Xiong Jian-Hang Leng Zhi-Yong Hu Department of Anesthesiology First Affiliated HospitalZhejiang University School of MedicineHangzhouZhejiang 310003China Department of Cell Biology Yale UniversityNew HavenCT 06520USA Department of Neurology of the First Affiliated Hospital Interdisciplinary Institute of Neuroscience and TechnologySchool of Brain Science and Brain MedicineZhejiang University School of MedicineHangzhouZhejiang 310027China Department of Anesthesiology Jiaxing Maternity and Childcare Health HospitalJiaxingZhejiang 314009China Department of Anesthesiology Penn State Hershey Medical CentrePenn State College of MedicineHersheyPA 17033USA Department of Central Laboratory Affiliated Hangzhou First People’s HospitalWestlake University School of MedicineHangzhouZhejiang 310006China

General anesthetic agents can impact brain function through interactions with neurons and their effects on glial cells.oligodendrocytes perform essential roles in the central nervous system,including myelin sheath formation,axonal metabolism,and neuroplasticity regulation.They are particularly vulnerable to the effects of general anesthetic agents resulting in impaired proliferation,differentiation,and apoptosis.Neurologists are increasingly interested in the effects of general anesthetic agents on oligodendrocytes.These agents not only act on the surface receptors of oligodendrocytes to elicit neuroinflammation through modulation of signaling pathways,but also disrupt metabolic processes and alter the expression of genes involved in oligodendrocyte development and function.In this review,we summarize the effects of general anesthetic agents on oligodendrocytes.We anticipate that future research will continue to explore these effects and develop strategies to decrease the incidence of adverse reactions associated with the use of general anesthetic agents.

关键词： oligodendrocytes General anesthetic agents Neurotoxicity Central nervous system Perioperative neurocognitive disorders

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The Protective Effects of Flavonoids from Scutellaria Baicalensis Georgi Stems and Leaves on Oligodendrocyte Damage Induced by Aβ_1-42

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Pharmacology & Pharmacy 2024年第1期15卷 1-13页

作者： Tangtang Song Yinhui Yao Yazhen Shang Institute of Traditional Chinese Medicine Chengde Medical College Chengde China Hebei Province Key Research Office of Traditional Chinese Medicine against Dementia Hebei Province Key Laboratory of Traditional Chinese Medicine Research and Development Hebei Key Laboratory of Nerve Injury and Repair Chengde China

Aim: This study aimed to investigate the protective effects of flavonoids from the stem and leaves of Scutellaria baicalensis Georgi (SSFs) against Aβ1-42-induced oligodendrocytes (OL) damage. Methods: Immunofluorescence was used for the detection of myelin-associated glycoprotein (MAG), a characteristic protein of rat oligodendrocytes (OLN-93 cells). To evaluate the potential protective effects of SSFs on OLN-93 cells injured by Aβ1-42, an injury model was established by subjecting OLN-93 cells to Aβ1-42 exposed. Cell morphology was examined using an inverted microscope, while cell viability was assessed using the colorimetric method of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT). Additionally, lactate dehydrogenase (LDH) was measured using the pyruvic acid reduction assay. The Ginkgo biloba leaf extract (GBE) injection was used as a positive control. Results: A total of >95% of the MAG immunofluorescence-positive cells were identified as oligodendrocytes. Gradually increasing concentrations of SSFs impaired the cells, and the maximum nondetrimental dose for OLN-93 cells was 75 mg/L. This study assessed the effects of SSFs on OLN-93 cells damaged by Aβ1-42. The results indicated that SSFs significantly improved OLN-93 cell morphological abnormal changes, increased the OLN-93 cell survival rate, and reduced LDH release. Conclusion: SSFs can alleviate Aβ1-42-induced damage of OL.

关键词： Flavonoids form the Stem and Leaves of Scutellaria baicalensis Georgi Aβ1-42 oligodendrocytes Damage

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Dysfunction of the oligodendrocytes in amyotrophic lateral sclerosis

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The Journal of Biomedical Research 2022年第5期36卷 336-342页

作者： Zhenxiang Gong Li Ba Min Zhang Department of Neurology and Psychiatry Tongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhanHubei 430030China

Amyotrophic lateral sclerosis(ALS)is a fatal neurodegenerative disorder characterized by irreversible deterioration of upper and lower motor neurons(MNs).Previously,studies on the involvement of glial cells in the pathogenic process of ALS have mainly revolved around astrocytes and microglia.And oligodendrocytes(OLs)have only recently been highlighted.Grey matter demyelination within the motor cortex and proliferation of the oligodendrocyte precursor cells(OPCs)was observed in ALS patients.The selective ablation of mutant SOD1(the dysfunctional superoxide dismutase)from the oligodendrocyte progenitors after birth significantly delayed disease onset and prolonged the overall survival in ALS mice model(SOD1G37R).In this study,we review the several mechanisms of oligodendrocyte dysfunction involved in the pathological process of myelin damage and MNs death during ALS.Particularly,we examined the insufficient local energy supply from OLs to axons,impaired differentiation from OPCs into OLs mediated by oxidative stress damage,and inflammatory injury to the OLs.Since increasing evidence depicted that ALS is not a disease limited to MNs damage,exploring the mechanisms by which oligodendrocyte dysfunction is involved in MNs death would contribute to a more comprehensive understanding of ALS and identifying potential drug targets.

关键词： oligodendrocytes amyotrophic lateral sclerosis energy metabolism oxidative stress neuroinflammation

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Three-dimensional bioprinting sodium alginate/gelatin scaffold combined with neural stem cells and oligodendrocytes markedly promoting nerve regeneration after spinal cord injury

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Regenerative Biomaterials 2022年第1期9卷 522-532页

作者： Shuo Liu Hui Yang Dong Chen Yuanyuan Xie ChenXu Tai Liudi Wang Peng Wang Bin Wang Clinical Stem Cell Center Nanjing Drum Tower Hospitalthe Affiliated Hospital of Nanjing University Medical SchoolNanjing 210000Jiangsu ProvinceChina State Key Laboratory of Pharmaceutical Biotechnology Department of Sports Medicine and Adult Reconstructive SurgeryNanjing Drum Tower HospitalThe Affiliated Hospital of Nanjing University Medical SchoolNanjing 210000Jiangsu ProvinceChina

Accumulating research has indicated that the transplantation of combined stem cells and scaffolds is an effective method for spinal cord injury(SCI).The development of three-dimensional(3D)bioprinting technology can make the 3D scaffolds combined with cells more accurate and effective for SCI treatment.However,unmyelinated newborn nerve fibers have no nerve signaling conduction,hampering recovery of motor function.In this study,we designed and printed a type of sodium alginate/gelatin scaffold loaded with neural stem cells and oligodendrocytes,which were involved in the formation of the myelin sheaths of neural cell axons.In order to observe the effectiveness of this 3D bioprinting scaffold,we transplanted it into the completely transected rat spinal cord,and then immunofluorescence staining,hematoxylin–eosin staining and behavioral assessment were performed.The results showed that this 3D bioprinting scaffold markedly improved the hindlimb motor function and promoted nerve regeneration.These findings suggested that this novel 3D bioprinting scaffold was a good carrier for cells transplantation,thereby enhancing spinal cord repair following injury.

关键词： three-dimensional bioprinting neural stem cell oligodendrocytes spinal cord injury

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Nogo-A aggravates oxidative damage in oligodendrocytes

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Neural Regeneration Research 2021年第1期16卷 179-185页

作者： Yang-Yang Wang Na Han Dao-Jun Hong Jun Zhang Department of Neurology Peking University People’s HospitalBeijingChina Department of Neurology The First Affiliated Hospital of Nanchang UniversityNanchangJiangxi ProvinceChina

Nogo-A is considered one of the most important inhibitors of myelin-associated axonal regeneration in the central nervous system.It is mainly expressed by oligodendrocytes.Although previous studies have found regulatory roles for Nogo-A in neurite outgrowth inhibition,neuronal homeostasis,precursor migration,plasticity,and neurodegeneration,its functions in the process of oxidative injury are largely uncharacterized.In this study,oligodendrocytes were extracted from the cerebral cortex of newborn Sprague-Dawley rats.We used hydrogen peroxide(H2O2)to induce an in vitro oligodendrocyte oxidative damage model and found that endogenously expressed Nogo-A is significantly upregulated in oligodendrocytes.After recombinant virus Ad-ZsGreen-rat Nogo-A infection of oligodendrocytes,Nogo-A expression was increased,and the infected oligodendrocytes were more susceptible to acute oxidative insults and exhibited a markedly elevated rate of cell death.Furthermore,knockdown of Nogo-A expression in oligodendrocytes by Ad-ZsGreen-shRNA-Nogo-A almost completely protected against oxidative stress induced by exogenous H2O2.Intervention with a Nogo-66 antibody,a LINGO1 blocker,or Y27632,an inhibitor in the Nogo-66-NgR/p75/LINGO-1-RhoA-ROCK pathway,did not affect the death of oligodendrocytes.Ad-ZsGreen-shRNA-Nogo-A also increased the levels of phosphorylated extracellular signal-regulated kinase 1/2 and inhibited BCL2 expression in oligodendrocytes.In conclusion,Nogo-A aggravated reactive oxygen species damage in oligodendrocytes,and phosphorylated extracellular signal-regulated kinase 1/2 and BCL2 might be involved in this process.This study was approved by the Ethics Committee of Peking University People’s Hospital,China(approval No.2018PHC081)on December 18,2018.

关键词： BCL2 H2O2 LINGO1 NgR Nogo-A oligodendrocytes phosphorylated extracellular signal-regulated kinase 1/2 reactive oxygen species

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Clemastine in remyelination and protection of neurons and skeletal muscle after spinal cord injury

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Neural Regeneration Research 2023年第5期18卷 940-946页

作者： Ali Myatich Azizul Haque Christopher Sole Naren L.Banik Department of Microbiology and Immunology Medical University of South CarolinaCharlestonSCUSA Department of Neurosurgery Medical University of South CarolinaCharlestonSCUSA Ralph H.Johnson Veterans Administration Medical Center CharlestonSCUSA Department of Health and Human Performance The CitadelCharlestonSCUSA

Spinal cord injuries affect nearly five to ten individuals per million every year. Spinal cord injury causes damage to the nerves, muscles, and the tissue surrounding the spinal cord. Depending on the severity, spinal injuries are linked to degeneration of axons and myelin, resulting in neuronal impairment and skeletal muscle weakness and atrophy. The protection of neurons and promotion of myelin regeneration during spinal cord injury is important for recovery of function following spinal cord injury. Current treatments have little to no effect on spinal cord injury and neurogenic muscle loss. Clemastine, an Food and Drug Administration-approved antihistamine drug, reduces inflammation, protects cells, promotes remyelination, and preserves myelin integrity. Recent clinical evidence suggests that clemastine can decrease the loss of axons after spinal cord injury, stimulating the differentiation of oligodendrocyte progenitor cells into mature oligodendrocytes that are capable of myelination. While clemastine can aid not only in the remyelination and preservation of myelin sheath integrity, it also protects neurons. However, its role in neurogenic muscle loss remains unclear. This review discusses the pathophysiology of spinal cord injury, and the role of clemastine in the protection of neurons, myelin, and axons as well as attenuation of skeletal muscle loss following spinal cord injury.

关键词： axonal damage clemastine myelination neuronal death oligodendrocytes skeletal muscle spinal cord injury

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CDP-choline to promote remyelination in multiple sclerosis:the need for a clinical trial

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Neural Regeneration Research 2023年第12期18卷 2599-2605页

作者： Viktoria Gudi PawełGrieb Ralf ALinker Thomas Skripuletz Department of Neurology Hannover Medical SchoolHannoverGermany Department of Experimental Pharmacology Mossakowski Medical Research InstitutePolish Academy of SciencesWarsawPoland Department of Neurology University Hospital RegensburgRegensburgGermany

Multiple sclerosis is a multifactorial chronic inflammatory disease of the central nervous system that leads to demyelination and neuronal cell death,resulting in functional disability.Remyelination is the natural repair process of demyelination,but it is often incomplete or fails in multiple sclerosis.Available therapies reduce the inflammatory state and prevent clinical relapses.However,therapeutic approaches to increase myelin repair in humans are not yet available.The substance cytidine-5′-diphosphocholine,CDP-choline,is ubiquitously present in eukaryotic cells and plays a crucial role in the synthesis of cellular phospholipids.Regenerative properties have been shown in various animal models of diseases of the central nervous system.We have already shown that the compound CDPcholine improves myelin regeneration in two animal models of multiple sclerosis.However,the results from the animal models have not yet been studied in patients with multiple sclerosis.In this review,we summarise the beneficial effects of CDP-choline on biolipid metabolism and turnover with regard to inflammatory and regenerative processes.We also explain changes in phospholipid and sphingolipid homeostasis in multiple sclerosis and suggest a possible therapeutic link to CDP-choline.

关键词： astrocytes CDP-choline cuprizone microglia multiple sclerosis oligodendrocytes

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Effects of neurotrophin-3 on the differentiation of neural stem cells into neurons and oligodendrocytes

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Neural Regeneration Research 2012年第19期7卷 1483-1487页

作者： Guowei Zhu Chongran Sun Weiguo Liu Department of Neurosurgery Second Affiliated Hospital of Zhejiang University Medical CollegeHangzhou 310009Zhejiang ProvinceChina

In this study, cells from the cerebral cortex of fetal rats at pregnant 16 days were harvested and cultured with 20 μg/L neurotrophin-3. After 7 days of culture, immunocytochemical staining showed that, 22.4% of cells were positive for nestin, 10.5% were positive for 18-111 tubulin （neuronal marker）, and 60.6% were positive for glial fibrillary acidic protein, but no cells were positive for 04 （oligodendrocytic marker）. At 14 days, there were 5.6% nestin-, 9.6% 13-111 tubulin-, 81.1% glial fibrillary acidic protein-, and 2.2% O4-positive cells. In cells not treated with neurotrophin-3, some were nestin-positive, while the majority showed positive staining for glial fibdllary acidic protein. Our experimental findings indicate that neurotrophin-3 is a crucial factor for inducing neural stem cells differentiation into neurons and oligodendrocytes.

关键词： neurotrophin-3 neural stem cells differentiation neuron oligodendrocytes stem cells neuralregeneration

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Immunological Markers for Central Nervous System Glia

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Neuroscience Bulletin 2023年第3期39卷 379-392页

作者： Hao Huang Wanjun He Tao Tang Mengsheng Qiu Zhejiang Key Laboratory of Organ Development and Regeneration Institute of Life SciencesCollege of Life and Environmental SciencesHangzhou Normal UniversityHangzhou 311121China Department of Anatomy Cell Biology and Physiology Stark Neurosciences Research InstituteIndiana University School of MedicineIndianapolisIN 46202USA

Glial cells in the central nervous system(CNS)are composed of oligodendrocytes,astrocytes and microglia.They contribute more than half of the total cells of the CNS,and are essential for neural development and functioning.Studies on the fate specification,differentiation,and functional diversification of glial cells mainly rely on the proper use of cell-or stage-specific molecular markers.However,as cellular markers often exhibit different specificity and sensitivity,careful consideration must be given prior to their application to avoid possible confusion.Here,we provide an updated overview of a list of well-established immunological markers for the labeling of central glia,and discuss the cell-type specificity and stage dependency of their expression.

关键词： Glial cells oligodendrocytes Astrocytes Microglia Markers

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Regulation of Glial Function by Noncoding RNA in Central Nervous System Disease

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Neuroscience Bulletin 2023年第3期39卷 440-452页

作者： Ying Bai Hui Ren Liang Bian You Zhou Xinping Wang Zhongli Xiong Ziqi Liu Bing Han Honghong Yao Department of Pharmacology Jiangsu Provincial Key LaboratorySchool of MedicineSoutheast UniversityNanjing 210009China Co-innovation Center of Neuroregeneration Nantong UniversityNantong 226001China Institute of Life Sciences Key Laboratory of Developmental Genes and Human DiseaseSoutheast UniversityNanjing 210009China

Non-coding RNAs(ncRNAs)are a class of functional RNAs that play critical roles in different diseases.NcRNAs include microRNAs,long ncRNAs,and circular RNAs.They are highly expressed in the brain and are involved in the regulation of physiological and pathophysiological processes of central nervous system(CNS)diseases.Mounting evidence indicates that ncRNAs play key roles in CNS diseases.Further elucidating the mechanisms of ncRNA underlying the process of regulating glial function that may lead to the identification of novel therapeutic targets for CNS diseases.

关键词： Noncoding RNA MicroRNA Long noncoding RNA Circular RNA Astrocytes Microglia oligodendrocytes

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