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Protective effects of dihydromyricetin on primary hippocampal astrocytes co-cultured with high glucose plus substance P and corticosterone

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Protective effects of dihydromyricetin on primary hippocampa...

小胶质细胞抑制剂在神经性疼痛和吗啡耐受中的调节机制和治疗潜力

2019中国生理学会学术年会暨张锡钧基金第十五届全国青...

作者：葛会香 Mengyun Sun Xingyu Wei Hongcheng Tu Ruxin Chen Miao Ye Cancan Yin Ruoyu Huang Wenhao Shen Wei Xiong Yun Gao Department of Physiology Basic Medical CollegeNanchang University Medical College of grade 2017 Nanchang University Affiliated Stomatological Hospital of Nanchang University Jiangxi Provincial Key Laboratory of Autonomic Nervous Function and Disease

Activated astrocytes are key players in diabetic neuropathic pain and depression.Dihydromyricetin（DHM） is a natural dihydroflavonoid.Our aim was to investigate whether DHM has a protective effect on the primary hippocampal astrocytes co-cultured with high glucose（HG）plus substance P（SP） and corticosterone（CORT）.Co-culture of HG+SP+CORT resulted in damage to the primary cultured hippocampal astrocytes, but DHM treatment could alleviate the impairment.Using qPCR, Western blot, immunofluorescence, We found that HG+SP+CORT increased the expression of P2 X7 receptor in primary cultured hippocampal astrocytes, whereas DHM treatment significantly reversed the change.Culture of the primary hippocampal astrocytes with HG+SP+CORT was able to elevate the level of TNF-α, IL-1β, free Ca 2+, and ERK1/2 phosphorylation.These increases could be inhibited by DHM or P2 X7 shRNA treatment.Furthermore, DHM significantly reduced the P2 X7 agonist activated currents in HEK293 cells transfected with the P2 X7 receptor.These findings suggest that DHM can protect the primary hippocampal astrocytes co-cultured with HG+SP+CORT form P2 X7 receptor-mediated damage.Co-culture of cells and HG+SP+CORT might be a good cell model for exploring pain and depression injury in diabetes mellitus.

关键词： Dihydromyricetin diabetic neuropathic pain depression primary culture hippocampal astrocyte P2X7 receptor

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Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2020年第3期21卷 204-217页

作者： Er-rong DU Rong-ping FAN Li-lou RONG Zhen XIE Chang-shui XU Department of Physiology Basic Medical College of Nanchang UniversityNanchang 330006China Department of Fourth Clinical Medicine School of MedicineNanchang UniversityNanchang 330006China Department of First Clinical Medicine School of MedicineNanchang UniversityNanchang 330006China key laboratory of autonomic nervous function and disease of jiangxi Province Nanchang 330006China

小胶质细胞是参与调节神经性疼痛(NPP)和吗啡耐受性的重要细胞。在确定它们的生理结构后,已经阐明了有关其可塑性和极性的信息,但关于这种类型的细胞在NPP和吗啡耐受性中的作用,仍有许多知识要学习。小胶质细胞通过控制中枢神经系统的... 详细信息

小胶质细胞是参与调节神经性疼痛(NPP)和吗啡耐受性的重要细胞。在确定它们的生理结构后,已经阐明了有关其可塑性和极性的信息,但关于这种类型的细胞在NPP和吗啡耐受性中的作用,仍有许多知识要学习。小胶质细胞通过控制中枢神经系统的损伤和对疾病的内源性免疫反应,介导健康和疾病的多种功能。小胶质细胞活化可导致阿片样物质系统活性改变,而NPP的特征在于对吗啡的抗性。在这里,我们研究小胶质细胞的调节机制,并综述了小胶质细胞抑制剂抑制NPP和吗啡耐受性的潜力。靶向的神经胶质活化是治疗NPP和预防吗啡耐受的临床有前途的方法。最后,我们为小胶质细胞抑制剂的未来研究提出了建议。

关键词：小胶质细胞神经性疼痛吗啡耐受小胶质细胞抑制剂

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

Effects of Fluvastatin on Characteristics of Stellate Ganglion Neurons in a Rabbit Model of Myocardial Ischemia

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Chinese Medical Journal 2016年第5期129卷 549-556页

作者： Li-Jun Cheng Guang-Ping Li Jian Li Yan Chen Xing-Hua Wang Tianjin key laboratory of Ionic-Molecular function of Cardiovascular disease Department of Cardiology Tianjin Institute of Cardiology Second Hospital of Tianjin Medical University Tianjin 300211 China

Background：Stellate ganglion （SG） plays an important role in cardiovascular diseases.The electrical activity of SG neurons is involved in the regulation of the autonomic nervous system.The aim of this research was to evaluate the effects offluvastatin on the electrophysiological characteristics of SG neurons in a rabbit model of myocardial ischemia （MI）.Methods：The MI model was induced by abdominal subcutaneous injections of isoproterenol in rabbits.Using whole-cell patch clamp technique,we studied the characteristic changes of ion channels and action potentials （APs） in isolated SG neurons in control group （n =20）,MI group （n =20） and fluvastatin pretreated group （fluvastatin group,n =20）,respectively.The protein expression of sodium channel in SG was determined by immunohistochemical analysis.Results：MI and the intervention of fluvastatin did not have significantly influence on the characteristics of delayed rectifier potassium channel currents.The maximal peak current density of sodium channel currents in SG neurons along with the characteristics of activation curves,inactivation curves,and recovery curves after inactivation were changed in the MI group.The peak current densities of control group,MI group,and fluvastatin group （n =10 in each group） were-71.77 ± 23.22 pA/pF,-126.75 ± 18.90 pA/pF,and-86.42 ± 28.30 pA/pF,respectively （F=4.862,P =0.008）.Fluvastatin can decrease the current amplitude which has been increased by MI.Moreover,fluvastatin induced the inactivation curves and post-inactive recovery curves moving to the position of the control group.But the expression of sodium channel-associated protein （Nav 1.7） had no significantly statistical difference among the three groups.The percentages of Nav 1.7 protein in control group,MI group,and fluvastatin group （n =5 in each group） were 21.49 ± 7.33%,28.53 ± 8.26%,and 21.64 ± 2.78%,respectively （F =1.495,P =0.275）.Moreover,MI reduced the electrical activity of AP and increased amplitude of AP,fluvastatin pretreatment could recover amplitude and electrical

关键词： Action Potential Delayed Rectifier Potassium Channel Fluvastatin： Myocardial Ischemia Sodium Channel Stellate Ganglion

A new anterograde trans-synaptic tracer based on Sindbis virus

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Neural Regeneration Research 2022年第12期17卷 2761-2764页

作者： Xiang-Wei Shi Fan Jia Pei Lyu Fu-Qiang Xu State key laboratory of Magnetic Resonance and Atomic and Molecular Physics Key Laboratory of Magnetic Resonance in Biological SystemsWuhan Center for Magnetic ResonanceInnovation Academy for Precision Measurement Science and TechnologyChinese Academy of SciencesWuhanHubei ProvinceChina Guangdong provincial key laboratory of Brain Connectome and Behavior CAS Key Laboratory of Brain Connectome and Manipulationthe Brain Cognition and Brain Disease Institute(BCBDI)Translational Research Center for the Nervous System(TRCNS)Shenzhen Institute of Advanced TechnologyChinese Academy of SciencesShenzhen-Hong Kong Institute of Brain Science-Shenzhen Fundamental Research InstitutionsShenzhenGuangdong ProvinceChina NMPA key laboratory for Research and Evaluation of Viral Vector Technology in Cell and Gene Therapy Medicinal Products Key Laboratory of Quality Control Technology for Virus-Based TherapeuticsGuangdong Provincial Medical Products AdministrationShenzhen Key Laboratory of Viral Vectors for BiomedicineShenzhen Institute of Advanced TechnologyChinese Academy of SciencesShenzhenGuangdong ProvinceChina University of Chinese Academy of Sciences BeijingChina Wuhan National laboratory for Optoelectronics Huazhong University of Science and TechnologyWuhanHubei ProvinceChina

Mapping neural circuits is critical for understanding the structure and function of the nervous system.Engineered viruses are a valuable tool for tracing neural circuits.However,current tracers do not fully meet the needs for this approach because of various drawbacks,such as toxicity and characteristics that are difficult to modify.Therefore,there is an urgent need to develop a new tracer with low toxicity and that allows for long-term studies.In this study,we constructed an engineered Sindbis virus(SINV)expressing enhanced green fluorescent protein(EGFP)reporter gene(SINV-EGFP)and found that it had no significant difference in biological characterization compared with the wild-type Sindbis virus in BHK-21 cells and neurons in vitro.We injected the virus into the visual circuit of mouse brain and found that the virus infected neurons in the local injected site and anterogradely spread in the neural circuits.Although the efficiency of transmission was limited,the findings demonstrate that SINV can be used as a new anterograde tracer to map neural circuits in mouse brain and that it spreads exclusively in the anterograde direction.Further,use of SINV in mouse brain research will provide longer time windows for circuit tracing than is possible with herpes simplex virus and vesicular stomatitis virus tracers.

关键词： anterograde lateral geniculate nucleus mouse brains neural circuit neurons retina Sindbis virus superior colliculus synapse tracer

Risk factors and causes of hyponatremia in patients after radiotherapy for head and neck cancer:A retrospective study

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Radiation Medicine and Protection 2021年第1期2卷 13-16页

作者： Yaxuan Pi Yi Li Zhongshan Shi Yamei Tang Department of Neurology Sun Yat-Sen Memorial HospitalSun Yat-Sen UniversityGuangzhou510120China Guangdong provincial key laboratory of Malignant Tumor Epigenetics and Gene Regulation Sun Yat-Sen Memorial HospitalSun Yat-Sen UniversityGuangzhou510120China Guangdong Province key laboratory of Brain function and disease Zhongshan School of MedicineSun Yat-Sen UniversityGuangzhou510120China

Background:Hyponatremia is the most frequently encountered electrolyte abnormality which is caused by kinds of reasons including kidney,metabolic and central nervous system diseases.The adverse effects of hyponatremia include but not limit to cerebral edema and seizures,which often aggravate neurological damage.Therefore,early diagnosis and intervention would reduce the risk of adverse effects of hyponatremia.Objective:To investigate the differences between patients with or without hyponatremia after radiotherapy for head and neck cancer,and to explore the risk factors and causes of hyponatremia.Methods:Patients who aged over 18 years old and underwent radiotherapy for head and neck cancer were collected from Department of Neurology,Sun Yat-Sen Memorial Hospital from January 2012 to July 2018.The comorbidities of patients and demographic and serological data were retrospectively collected to investigate the causes and risk factors of hyponatremia in these patients.Differences of the length of hospital stay and the cognitive function between patients with and without hyponatremia were analyzed.Results:In this study,798 patients were reviewed.The incidence of hyponatremia was 17.9%.Risk factors of hyponatremia included age(OR 1.05,95%CI 1.03–1.07,P<0.001),gender(OR 0.62,95%CI 0.39–0.99,P=0.046),medical history of hypothyroidism(OR 2.42,95%CI 1.26–4.09,P紏0.006),adrenal insufficiency(OR 15.61,95%CI 2.73–89.07,P=0.002)or dysphagia(OR 1.81,95%CI 1.24–2.65,P=0.002).The most common cause of hyponatremia was cerebral salt-wasting syndrome(CSWS)(32.9%).The insufficient intake due to dysphagia(29.4%),and hypothyroidism(13.3%)were also common in these patients.Clinically,hyponatremia resulted in the prolonged hospitalization time.Conclusion:Hyponatremia would be common in patients who underwent radiotherapy for head and neck cancer.The importance of distinguishing the etiology of hyponatremia is addressed.

关键词： Hyponatremia Head and neck cancer Radiotherapy Cerebral salt-wasting syndrome

Epigenetic and transcriptional activation of the secretory kinase FAM20C as an oncogene in glioma

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Journal of Genetics and Genomics 2023年第6期50卷 422-433页

作者： Bo Gong Yi Liang Qian Zhang Huan Li Jialing Xiao Liang Wang Han Chen Wenjie Yang Xiaoqing Wang Yi Wang Zongze He Department of Health Management Sichuan Provincial People's HospitalUniversity of Electronic Science and Technology of ChinaChengduSichuan 610072China The key laboratory for Human disease Gene Study of Sichuan Province and Institute of laboratory Medicine Sichuan Provincial People's HospitalUniversity of Electronic Science and Technology of ChinaChengduSichuan 610072China Department of Neurology Sichuan Provincial People's HospitalUniversity of Electronic Science and Technology of ChinaChengduSichuan 610072China Department of Neurosurgery Sichuan Provincial People's HospitalUniversity of Electronic Science and Technology of ChinaChengduSichuan 610072China Department of Pathology Sichuan Provincial People's HospitalUniversity of Electronic Science and Technology of ChinaChengduSichuan 610072China Department of Critical Care Medicine Sichuan Provincial People's HospitalUniversity of Electronic Science and Technology of ChinaChengduSichuan610072China

Gliomas are the most prevalent and aggressive malignancies of the nervous system.Previous bioinformatic studies have revealed the crucial role of the secretory pathway kinase FAM20C in the prediction of glioma invasion and malignancy.However,little is known about the pathogenesis of FAM20C in the regulation of glioma.Here,we construct the full-length transcriptome atlas in paired gliomas and observe that 22 genes are upregulated by full-length transcriptome and differential APA analysis.Analysis of ATAC-seq data reveals that both FAM20C and NPTN are the hub genes with chromatin openness and differential expression.Further,in vitro and in vivo studies suggest that FAM20C stimulates the proliferation and metastasis of glioma cells.Meanwhile,NPTN,a novel cancer suppressor gene,counteracts the function of FAM20C by inhibiting both the proliferation and migration of glioma.The blockade of FAM20C by neutralizing antibodies results in the regression of xenograft tumors.Moreover,MAX,BRD4,MYC,and REST are found to be the potential trans-active factors for the regulation of FAM20C.Taken together,our results uncover the oncogenic role of FAM20C in glioma and shed new light on the treatment of glioma by abolishing FAM20C.

关键词： Glioma Alternativepolyadenylation sites FAM20C Trans-activefactors

CircFhit Modulates GABAergic Synaptic Transmission via Regulating the Parental Gene Fhit Expression in the Spinal Dorsal Horn in a Rat Model of Neuropathic Pain

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Neuroscience Bulletin 2023年第6期39卷 947-961页

作者： Ting Xu Zhen-Yu Li Meng Liu Su-Bo Zhang Huan-Huan Ding Jia-Yan Wu Su-Yan Lin Jun Liu Jia-You Wei Xue-Qin Zhang Wen-Jun Xin Neuroscience Program of Zhongshan School of Medicine and the Fifth Affiliated Hospital Sun Yat-sen UniversityGuangzhou510080China Guangdong Province key laboratory of Brain function and disease Sun Yat-sen UniversityGuangzhou510120China Department of Anesthesia and Pain Medicine Guangzhou First People’s HospitalGuangzhou510000China Department of Physiology Xuzhou Medical UniversityXuzhou221004China Department of Neurology The Second Affiliated HospitalGuangzhou Medical UniversityGuangzhou510000China Guangdong provincial Engineering Research Center of Molecular Imaging Guangdong Provincial Key Laboratory of Biomedical Imagingand Department of Interventional MedicineThe Fifth Affiliated HospitalSun Yat-sen UniversityZhuhai519000China The Affiliated Brain Hospital(Guangzhou Huiai Hospital)and School of Health Management Guangzhou Medical UniversityGuangzhou510182China Guangdong-Hong Kong-Macao Greater Bay Area Center for Brain Science and Brain-Inspired Intelligence Guangzhou510000China

Effective treatments for neuropathic pain are lacking due to our limited understanding of the mechanisms.The circRNAs are mainly enriched in the central nervous system.However,their function in various physiological and pathological conditions have yet to be determined.Here,we identified circFhit,an exon-intron circRNA expressed in GABAergic neurons,which reduced the inhibitory synaptic transmission in the spinal dorsal horn to mediate spared nerve injury-induced neuropathic pain.Moreover,we found that circFhit decreased the expression of GAD65 and induced hyperexcitation in NK1R^(+) neurons by promoting the expression of its parental gene Fhit in cis.Mechanistically,circFhit was directly bound to the intronic region of Fhit,and formed a circFhit/HNRNPK complex to promote Pol II phosphorylation and H2B monoubiquitination by recruiting CDK9 and RNF40 to the Fhit intron.In summary,we revealed that the exon-intron circFhit contributes to GABAergic neuron-mediated NK1R^(+) neuronal hyperexcitation and neuropathic pain via regulating Fhit in cis.

关键词： Chronic pain Neuropathic pain CircRNA Inhibitory transmission Epigenetic regulation

The clinical features and potential mechanisms of cognitive disorders in peripheral autoimmune and inflammatory diseases

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Fundamental Research 2024年第2期4卷 226-236页

作者： Ke-qi Fan Tao Huang Jian-shuai Yu Yi-yuan Li Jin Jin MOE laboratory of Biosystem Homeostasis and Protection and Life Sciences InstituteZhejiang UniversityHangzhou 310058China Department of Gastroenterology Sir Run Shaw HospitalCollege of Medicine Zhejiang UniversityHangzhou 310016China key laboratory for Developmental Genes and Human disease Ministry of EducationInstitute of Life SciencesJiangsu Province High-Tech Key Laboratory for Bio-Medical ResearchSoutheast UniversityNanjing 210096China

According to a study from World Health Organization’s Global Burden of disease,mental and neurological disorders have accounted for 13%of global diseases in recent years and are on the rise.Neuropsychiatric conditions or neuroinflammatory disorders are linked by the presence of an exaggerated immune response both peripherally and in the central nervous system(CNS).Cognitive dysfunction(CD)encompasses a complex group of diseases and has frequently been described in the field of autoimmune diseases,especially in multiple non-CNS-related autoimmune diseases.Recent studies have provided various hypotheses regarding the occurrence of cognitive impairment in autoimmune diseases,including that abnormally activated immune cells can disrupt the integrity of the blood-brain barrier(BBB)to trigger a central neuroinflammatory response.When the BBB is intact,autoantibodies and pro-inflammatory molecules in peripheral circulation can enter the brain to activate microglia,inducing CNS inflammation and CD.However,the mechanisms explaining the association between the immune system and neural function and their contribution to diseases are uncertain.In this review,we used clinical statistics to illustrate the correlation between CD and autoimmune diseases that do not directly affect the CNS,summarized the clinical features and mechanisms by which autoimmune diseases trigger cognitive impairment,and explored existing knowledge regarding the link between CD and autoimmune diseases from the perspective of the field of neuroimmunology.

关键词： Autoimmune diseases Neuroinflammation Central nervous system dysfunction Autoantibodies Inflammatory cytokines