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Identification of α7 nicotinic acetylcholine receptor on hippocampal astrocytes cultured in vitro and its role on inflammatory mediator secretion

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Neural Regeneration Research 2012年第22期7卷 1709-1714页

作者： Yan Wang Ning Zhu Kewan Wang Zhongyi Zhang Yong Wang Department of Pharmacy Zhujiang Hospital Southern Medical University Guangzhou 510282 Guangdong Province China Department of Pharmacy the 458 Hospital of Chinese PLA Guangzhou 510602 Guangdong Province China Department of Neurosurgery Nanfang Hospital Southern Medical University Guangzhou 510602 Guangdong Province China

The present study found expressions of a7 nicotinic acetylcholine receptor on hippocampal slices and hippocampal astrocytes using double immunofluorescence stainings. Expression of glial fibdllary acidic protein in the cultured hippocampal slices and hippocampal astrocytes significantly increased, and levels of macrophage inflammatory protein la, RANTES, interleukin-1β, intedeukin-6, and tumor necrosis factor-α increased in the supernatant of cultured astrocytes following exposure to 200 nM amyloid 13 protein 1-42. Preconditioning of 10 μM nicotine, a nicotinic acetylcholine receptor agonist, could attenuate the influence of amyloid β protein 1-42 in inflammatory mediator secretion of cultured astrocytes. Experimental findings indicated that α7 nicotinic acetylcholine receptor was expressed on the surface of hippocampal astrocytes, and activated a7 nicotinic acetylcholine receptor was shown to inhibit inflammation induced by amyloid β protein 1-42.

关键词： α7 nicotinic acetylcholine receptor astrocytes inflammation cytokines chemotactic factor amyloidβ protein hippocampus neural regeneration

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nicotinic acetylcholine receptorα7 subunit:a novel therapeutic target for cardiovascular diseases

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Frontiers of Medicine 2012年第1期6卷 35-40页

作者： Chong Liu Dingfeng Su Department of Pharmacology Second Military Medical UniversityShanghai 200433China

Inflammation is important in the pathogenesis and development of cardiovascular *** studies show that vagus nerve stimulation inhibits pro-inflammatory cytokine production through“the cholinergic anti-inflammatory pathway,”more specifically via theα7 nicotinic acetylcholine receptor(α7nAChR).In the current study,the role of the cholinergic anti-inflammatory pathway during septic shock,hypertension,and myocardial infarction is reviewed,and its possible clinical implications in cardiovascular diseases are discussed.

关键词： α7 nicotinic acetylcholine receptor cardiovascular diseases baroreflex sensitivity

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Vagus nerve stimulation is a potential treatment for ischemic stroke

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Neural Regeneration Research 2023年第4期18卷 825-831页

作者： Yi-Lin Liu San-Rong Wang Jing-Xi Ma Le-Hua Yu Gong-Wei Jia Department of Rehabilitation The Second Affiliated Hospital of Chongqing Medical UniversityChongqingChina The Second Clinical College Chongqing Medical UniversityChongqingChina Department of Neurology Chongqing General HospitalChongqingChina Chongqing Key Laboratory of Neurodegenerative Diseases ChongqingChina

Microglia are the brain’s primary innate immune cells,and they are activated and affect pro-inflammatory phenotype or regulatory phenotype after ischemic *** nerve stimulation was shown to activate microglial phenotypic changes and exhibit neuroprotective effects in ischemia/reperfusion *** this study,we established rat models of ischemic stroke by occlusion of the middle cerebral artery and performed vagus nerve stimulation 30 minutes after *** found that vagus nerve stimulation caused a shift from a pro-inflammatory phenotype to a regulatory phenotype in microglia in the ischemic *** nerve stimulation decreased the levels of pro-inflammatory phenotype markers inducible nitric oxide synthase and tumor necrosis factorαand increased the expression of regulatory phenotype markers arginase 1 and transforming growth factorβthrough activatingα7 nicotinic acetylcholine receptor ***,α7 nicotinic acetylcholine receptor blockade reduced the inhibition of Toll-like receptor 4/nuclear factor kappa-B pathwayassociated proteins,including Toll-like receptor 4,myeloid differentiation factor 88,I kappa B alpha,and phosphorylated-I kappa B alpha,and also weakened the neuroprotective effects of vagus nerve stimulation in ischemic *** nerve stimulation inhibited Toll-like receptor 4/nuclear factor kappa-B expression through activatingα7 nicotinic acetylcholine receptor and regulated microglial polarization after ischemic stroke,thereby playing a role in the treatment of ischemic *** from this study confirm the mechanism underlying vagus nerve stimulation against ischemic stroke.

关键词： cerebral ischemia microglia neuroprotection nuclear factor kappa-B pro-inflammatory phenotype regulatory phenotype reperfusion Toll-like receptor 4 vagus nerve stimulation α7 nicotinic acetylcholine receptor

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Vagus nerve stimulation protects against cerebral injury after cardiopulmonary resuscitation by inhibiting inflammation through the TLR4/NF-κB and α7nAChR/JAK2 signaling pathways

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World Journal of Emergency Medicine 2023年第6期14卷 462-470页

作者： Shuang Xu Lang Guo Weijing Shao Licai Liang Tingting Shu Yuhan Zhang He Huang Guangqi Guo Qing Zhang Peng Sun Department of Emergency Medicine Union HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430022China Department of Urology the Second Affiliated Hospital of Guangzhou University of Chinese MedicineGuangzhou 51000China Department of Emergency Medicine the Second Affiliated Hospital of Zhejiang University School of MedicineHangzhou 310009China Department of Intensive Care Unit Wuhan Hospital of Traditional Chinese MedicineWuhan 430000China Department of Intensive Care Unit Xiangyang Central HospitalAffiliated Hospital of Hubei University of Arts and ScienceXiangyang 441021China Department of Emergency General Hospital of Central Theatre Command of the Chinese People's Liberation ArmyWuhan 430070China Department of Anesthesiology Union HospitalTongji Medical CollegeHuazhong University of Science and Technology Wuhan 430022China

BACKGROUND: Our previous research proved that vagus nerve stimulation(VNS) improved the neurological outcome after cardiopulmonary resuscitation(CPR) by activating α7 nicotinic acetylcholine receptor(α7nAChR) in a rat model, but the underlying mechanism of VNS in neuroprotection after CPR remains ***: In vivo, we established a mouse model of cardiac arrest(CA)/CPR to observe the survival rate, and the changes in inflammatory factors and brain tissue after VNS treatment. In vitro, we examined the effects of α7nAChR agonist on ischemia/reperfusion(I/R)-induced inflammation in BV2 cells under oxygen-glucose deprivation/reoxygenation(OGD/R) conditions. We observed the changes in cell survival rate, the levels of inflammatory factors, and the expressions of α7nAChR/Janus kinase 2(JAK2) and toll-like receptor 4(TLR4)/nuclear factor-κB(NF-κB).RESULTS: In vivo, VNS preconditioning enhanced functional recovery, improved the survival rate, and reduced hippocampal CA1 cell damage, and the levels of inflammatory mediators after CA/CPR. The application of α7nAChR agonists provided similar effects against cerebral injury after the return of spontaneous circulation(ROSC), while α7nAChR antagonists reversed these neuroprotective impacts. The in vitro results mostly matched the findings in vivo. OGD/R increased the expression of tumor necrosis factor-alpha(TNF-α), TLR4 and NF-κB p65. When nicotine was added to the OGD/R model, the expression of TLR4, NF-κB p65, and TNF-α decreased, while the phosphorylation of JAK2 increased, which was prevented by preconditioning with α7nAChR or JAK2 ***: The neuroprotective effect of VNS correlated with the activation of α7nAChR. VNS may alleviate cerebral IR injury by inhibiting TLR4/NF-κB and activating the α7nAChR/JAK2 signaling pathway.

关键词： Cardiopulmonary resuscitation Vagus nerve stimulation Inflammation Toll-like receptor 4 α7 nicotinic acetylcholine receptor

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Mesenchymal stem cells as a potential therapeutic tool to cure cognitive impairment caused by neuroinflammation

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World Journal of Stem Cells 2021年第8期13卷 1072-1083页

作者： Maryna Skok Department of Molecular Immunology Palladin Institute of Biochemistry NAS of UkraineKyiv 01054Ukraine

An established contribution of neuroinflammation to multiple brain pathologies has raised the requirement for therapeutic strategies to overcome it in order to prevent age-and disease-dependent cognitive *** stem cells(MSCs)produce multiple growth and neurotrophic factors and seem to evade immune rejection due to low expression of major histocompatibility complex class I ***,MSCs are widely used in experiments and clinical trials of regenerative *** review summarizes recent data concerning the optimization of MSC use for therapeutic purposes with the emphasis on the achievements of the last 2 *** attention is paid to extracellular vesicles secreted by MSCs and to the role ofα7 nicotinic acetylcholine *** reviewed data demonstrate that MSCs have a significant therapeutic potential in treating neuroinflammation-related cognitive disfunctions including age-related neurodegenerative *** novel data demonstrate that maximal therapeutic effect is being achieved when MSCs penetrate the brain and produce their stimulating factors in ***,therapeutic application using MSCs should include measures to facilitate their homing to the brain,support the survival in the brain microenvironment,and stimulate the production of neurotrophic and anti-inflammatory *** measures include but are not limited to genetic modification of MSCs and pre-conditioning before transplantation.

关键词： Mesenchymal stem cells Neuroinflammation Cognition α7 nicotinic acetylcholine receptor Extracellular vesicles Alzheimer disease

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