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Recombinant adeno-associated virus 8-mediated inhibition of microRNA let-7a ameliorates sclerosing cholangitis in a clinically relevant mouse model

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World Journal of Gastroenterology 2024年第5期30卷 471-484页

作者： Hui Hua Qian-Qian Zhao Miriam Nkesichi Kalagbor Guo-Zhi Yu Man Liu Zheng-Rui Bian Bei-Bei Zhang Qian Yu Yin-Hai Xu Ren-Xian Tang Kui-Yang Zheng Chao Yan Jiangsu Key Laboratory of Immunity and Metabolism Department of Pathogenic Biology and ImmunologyNational Demonstration Center for Experimental Basic Medical Science EducationLaboratory of Infection and ImmunityXuzhou Medical UniversityXuzhou 221004Jiangsu ProvinceChina department of Laboratory Medicine The Affiliated Hospital of Xuzhou Medical UniversityXuzhou 221002Jiangsu ProvinceChina

BACKGROUND Primary sclerosing cholangitis(PSC)is characterized by chronic inflammation and it predisposes to cholangiocarcinoma due to lack of effective treatment *** adeno-associated virus(rAAV)provides a promising platform for gene therapy on such kinds of diseases.A microRNA(miRNA)let-7a has been reported to be associated with the progress of PSC but the potential therapeutic implication of inhibition of let-7a on PSC has not been *** To investigate the therapeutic effects of inhibition of a miRNA let-7a transferred by recombinant adeno-associated virus 8(rAAV8)on a xenobiotic-induced mouse model of sclerosing *** A xenobiotic-induced mouse model of sclerosing cholangitis was induced by 0.1% 3,5-Diethoxycarbonyl-1,4-Dihydrocollidine(DDC)feeding for 2 wk or 6 wk.A single dose of rAAV8-mediated anti-let-7a-5p sponges or scramble control was injected in vivo into mice onset of DDC *** sacrifice,the liver and the serum were collected from each *** hepatobiliary injuries,hepatic inflammation and fibrosis were *** targets of let-7a-5p and downstream molecule NF-κB were detected using Western *** rAAV8-mediated anti-let-7a-5p sponges can depress the expression of let-7a-5p in mice after DDC feeding for 2 wk or 6 *** reduced expression of let-7a-5p can alleviate hepato-biliary injuries indicated by serum markers,and prevent the proliferation of cholangiocytes and biliary ***,inhibition of let-7a mediated by rAAV8 can increase the expression of potential target molecules such as suppressor of cytokine signaling 1 and Dectin1,which consequently inhibit of NF-κB-mediated hepatic *** Our study demonstrates that a rAAV8 vector designed for liver-specific inhibition of let-7a-5p can potently ameliorate symptoms in a xenobiotic-induced mouse model of sclerosing cholangitis,which provides a possible clinical translation of PSC of human.

关键词： Primary sclerosing cholangitis Recombinant adeno-associated virus 8 Let-7a-5p Therapeutic effects Inflammation

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Newcastle disease virus suppresses antigen presentation via inhibiting IL-12 expression in dendritic cells

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Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2024年第3期25卷 254-270页

作者： Fulong NAN Wenlong NAN Xin YAN Hui WANG Shasha JIANG Shuyun ZHANG Zhongjie YU Xianjuan ZHANG Fengjun LIU Jun LI Xiaoqiong ZHOU Delei NIU Yiquan LI Wei WANG Ning SHI Ningyi JIN Changzhan XIE Xiaoni CUI He ZHANG Bin WANG Huijun LU department of Special Medicine Department of Pathogenic BiologySchool of Basic MedicineQingdao UniversityQingdao 266071China China Animal Health and Epidemiology Center Qingdao 266032China Academician Workstation of Jilin Province Changchun University of Chinese MedicineChangchun 130117China Institute of Virology Wenzhou UniversityWenzhou 325035China College of Veterinary Medicine Jilin UniversityChangchun 130012China Changchun Veterinary Research Institute Chinese Academy of Agricultural SciencesChangchun 130122China Sino-Cell Biomed Co. Ltd.Qingdao 266000China

As a potential vectored vaccine,Newcastle disease virus(NDV)has been subject to various studies for vaccine development,while relatively little research has outlined the immunomodulatory effect of the virus in antigen *** elucidate the key inhibitory factor in regulating the interaction of infected dendritic cells(DCs)and T cells,DCs were pretreated with the NDV vaccine strain LaSota as an inhibitor and stimulated with lipopolysaccharide(LPS)for further detection by enzyme-linked immunosorbent assay(ELISA),flow cytometry,immunoblotting,and quantitative real-time polymerase chain reaction(qRT-PCR).The results revealed that NDV infection resulted in the inhibition of interleukin(IL)-12p40 in DCs through a p38 mitogen-activated protein kinase(MAPK)-dependent manner,thus inhibiting the synthesis of IL-12p70,leading to the reduction in T cell proliferation and the secretion of interferon-(IFN-),tumor necrosis factor-α(TNF-α),and IL-6 induced by ***,downregulated cytokines accelerated the infection and viral transmission from DCs to T ***,several other strains of NDV also exhibited inhibitory *** current study reveals that NDV can modulate the intensity of the innate-adaptive immune cell crosstalk critically toward viral invasion improvement,highlighting a novel mechanism of virus-induced immunosuppression and providing new perspectives on the improvement of NDV-vectored vaccine.

关键词： Newcastle disease virus Dendritic cells Interleukin-12(IL-12) T cells Immunosuppression

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Attenuation of the Activation of NLRP3 Inflammasome in Fibroblast Like Synoviocytes of Rheumatoid Arthritis by Baicalin through Regulating the Let-7i-3p/PI3K/Akt/NF-κB Signaling Axis

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Medicinal Plant 2024年第2期15卷 69-73,76页

作者： Wei ZHANG Li WANG Yuxin YANG Rui MA Li WANG Ling HUANG Qiaofeng WAN department of pathogenic Biology and Immunology School of Basic MedicineNingxia Medical UniversityYinchuan 750004China department of Rheumatology Ningxia Medical University General HospitalYinchuan 750003China School of Clinical Medicine Ningxia Medical UniversityYinchuan 750004China

[Objectives]To study the effect and mechanism of baicalin on the activation of NLRP3 inflammasome in human fibroblast like synoviocytes of rheumatoid arthritis(HFLS-RA).[Methods]To confirm that baicalin alleviated the activation of NLRP3 inflammasome in HFLS-RA,the expression of NLRP3 before and after baicalin treatment was observed by *** blot was used to detect the protein expression of p-PI3K,p-Akt,NF-κB p65,NLRP3,ASC and caspase-1 after baicalin treatment for 48 h,and the contents of IL-1 and IL-18 in the supernatents were detected by *** order to explore the mechanism of baicalin alleviating the activation of NLRP3 inflammasome,the corresponding relationship between let-7i-3p and PIK3CA was verified by double luciferin and Westen blot *** expression of let-7i-3p and PI3K before and after baicalin intervention was detected by ***-7i-3p interference was used to verify whether baicalin mitigated the activation of enhanced NLRP3 inflammasome.[Results]Baicalin(50 and 100 mg/L)significantly reduced the activation of NLRP3 inflammasome,inhibited the protein expressions of p-PI3K,p-Akt,NF-κB p65,NLRP3,ASC and caspase-1,and the secretion of IL-1 and ***-7i-3p and PIK3CA had a targeted correspondence,and baicalin up-regulated the expression of let-7i-3p and down-regulated the expression of *** attenuated the activation of NLRP3 inflammasome enhanced by let-7i-3p interference.[Conclusions]Baicalin can up-regulate let-7i-3p expression,inhibit PI3K/Akt/NF-κB signal transduction,and thus reduce the activation of NLRP3 inflammasome in HFLS-RA.

关键词： Baicalin Rheumatoid arthritis Human fibroblast like synoviocytes of rheumatoid arthritis NLRP3 inflammasome miRNA Dual-luciferase

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Mechanistic research:Selenium regulates virulence factors,reducing adhesion ability and inflammatory damage of Helicobacter pylori

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World Journal of Gastroenterology 2024年第1期30卷 91-107页

作者： Chun Qin Gan-Rong Huang Ai-Xing Guan Wen-Ting Zhou Hao Chen Pei-Pei Luo Xian-Ke Luo Yan-Qiang Huang Zan-Song Huang Guangxi Technology Innovation Cooperation Base of Prevention and Control pathogenic Microbes with Drug Resistance Youjiang Medical University for NationalitiesBaise 533000Guangxi Zhuang Autonomous RegionChina department of Digestive Diseases Affiliated Hospital of Youjiang Medical University for NationalitiesBaise 533000Guangxi Zhuang Autonomous RegionChina Key Laboratory of the Prevention and Treatment of Drug Resistant Microbial Infecting Youjiang Medical University for NationalitiesBaise 533000Guangxi Zhuang Autonomous RegionChina department of Pathology Wannan Medical CollegeWuhu 241002Anhui ProvinceChina department of Gastroenterology Wujin People’s Hospital affiliated to Jiangsu UniversityChangzhou 213004Jiangsu ProvinceChina department of Gastroenterology Guangzhou Liwan District People's HospitalGuangzhou 510370Guangdong ProvinceChina

BACKGROUND The pathogenicity of Helicobacter pylori is dependent on factors including the environment and the *** selenium is closely related to pathogenicity as an environmental factor,the specific correlation between them remains *** To investigate how selenium acts on virulence factors and reduces their *** *** strains were induced by sodium *** expression of cytotoxin-associated protein A(CagA)and vacuolating cytotoxin gene A(VacA)was determined by quantitative PCR and Western *** was used to analyze CagA,CagM,CagE,Cag1,Cag3,and CagT.C57BL/6A mice were infected with the attenuated strains subjected to sodium selenite induction,and *** colonization,inflammatory reactions,and the cell adhesion ability of *** were *** CagA and VacA expression was upregulated at first and then downregulated in the *** strains after sodium selenite *** expression was significantly and steadily downregulated after the 5th cycle(10 d).Transcriptome analysis revealed that sodium selenite altered the levels affect *** virulence factors such as CagA,CagM,CagE,Cag1,Cag3,and *** these factors,CagM and CagE expression was continuously downregulated and further downregulated after 2 h of induction with sodium ***,CagT expression was upregulated before the 3rd cycle(6 d)and significantly downregulated after the 5th ***1 and Cag3 expression was upregulated and downregulated,respectively,but no significant change was observed by the 5th cycle.C57BL/6A mice were infected with the attenuated strains subjected to sodium selenite *** extent of *** colonization in the stomach increased;however,sodium selenite also induced a mild inflammatory reaction in the gastric mucosa of ***-infected mice,and the cell adhesion ability of *** was significantly *** These results demonstrate that *** displayed virulence attenuation after

关键词： Helicobacter pylori Sodium selenite Virulence factors Adherence Inflammation

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Lecithin-cholesterol acyltransferase is a potential tumor suppressor and predictive marker for hepatocellular carcinoma metastasis

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World Journal of Gastrointestinal Oncology 2024年第8期16卷 3651-3671页

作者： Yan Li Li-Na Jiang Bo-Kang Zhao Mei-Ling Li Yi-Yun Jiang Yi-Si Liu Shu-Hong Liu Li Zhu Xin Ye Jing-Min Zhao department of Pathology and Hepatology The Fifth Medical Center of Chinese PLA General HospitalBeijing 100039China department of Hepatology Center of Infectious Diseases and Pathogen BiologyThe First Hospital of Jilin UniversityChangchun 130061Jilin ProvinceChina First department of Liver Disease Center Beijing Youan HospitalCapital Medical UniversityBeijing 100069China Key Laboratory of pathogenic Microbiology and Immunology Institute of MicrobiologyChinese Academy of SciencesBeijing 100101China Savaid Medical School University of Chinese Academy of SciencesBeijing 100190China department of Pathology The Fifth Medical Center of Chinese PLA General HospitalBeijing 100039China

BACKGROUND Hepatocellular carcinoma(HCC)is a major cause of cancer mortality worldwide,and metastasis is the main cause of early recurrence and poor ***,the mechanism of metastasis remains poorly *** To determine the possible mechanism affecting HCC metastasis and provide a possible theoretical basis for HCC *** The candidate molecule lecithin-cholesterol acyltransferase(LCAT)was screened by gene microarray and bioinformatics *** expression levels of LCAT in clinical cohort samples was detected by quantitative realtime polymerase chain reaction and western *** proliferation,migration,invasion and tumor-forming ability were measured by Cell Counting Kit-8,Transwell cell migration,invasion,and clonal formation assays,*** formation was detected in nude mice after LCAT gene knockdown or *** immunohistochemistry for Ki67,E-cadherin,N-cadherin,matrix metalloproteinase 9 and vascular endothelial growth factor were performed in liver tissues to assess the effect of LCAT on *** set enrichment analysis(GSEA)on various gene signatures were analyzed with GSEA version *** machine-learning algorithms(random forest,support vector machine,and logistic regression)were applied to predict HCC metastasis in The Cancer Genome Atlas and GEO *** LCAT was identified as a novel gene relating to HCC metastasis by using gene microarray in HCC *** was significantly downregulated in HCC tissues,which is correlated with recurrence,metastasis and poor outcome of HCC *** analysis indicated that LCAT inhibited HCC cell proliferation,migration and invasion both in vitro and in *** data showed that LCAT was negatively associated with HCC size and metastasis(HCC size≤3 cm vs 3-9 cm,P9 cm,P<0.01;metastatic-free HCC vs extrahepatic metastatic HCC,P<0.05).LCAT suppressed the growth,migration and invasion of HCC cell lines via PI3K/A

关键词： Lecithin-cholesterol acyltransferase Tumor suppressor gene Hepatocellular carcinoma PI3K/AKT/mTOR Predicting model

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Targeting PKM2 signaling cascade with salvianic acid A normalizes tumor blood vessels to facilitate chemotherapeutic drug delivery

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Acta Pharmaceutica Sinica B 2024年第5期14卷 2077-2096页

作者： Cheng Qian Yueke Zhou Teng Zhang Guanglu Dong Mengyao Song Yu Tang Zhonghong Wei Suyun Yu Qiuhong Shen Wenxing Chen Jaesung P.Choi Juming Yan Chongjin Zhong Li Wan Jia Li Aiyun Wang Yin Lu Yang Zhao Jiangsu Key Laboratory for Pharmacology and Safety Evaluation of Chinese Materia Medica Nanjing University of Chinese MedicineNanjing 210023China School of Medicine&Holistic Integrative Medicine Nanjing University of Chinese MedicineNanjing 210023China Centre for Inflammation Faculty of ScienceCentenary InstituteSchool of Life SciencesUniversity of Technology SydneySydney NSW 2050Australia Jiangsu Key Laboratory of Immunity and Metabolism Department of Pathogenic Biology and ImmunologyNational Experimental Demonstration Center for Basic Medicine EducationXuzhou Laboratory of Infection and ImmunityXuzhou Medical UniversityXuzhou 221004China department of General Surgery Jiangsu Province Hospital of Chinese MedicineAffiliated Hospital of Nanjing University of Chinese MedicineNanjing 210029China Macquarie Medical School Faculty of MedicineHuman Health SciencesMacquarie UniversitySydney NSW 2109Australia

Aberrant tumor blood vessels are prone to propel the malignant progression of tumors,and targeting abnormal metabolism of tumor endothelial cells emerges as a promising option to achieve vascular normalization and antagonize tumor ***,we demonstrated that salvianic acid A(SAA)played a pivotal role in contributing to vascular normalization in the tumor-bearing mice,thereby improving delivery and effectiveness of the chemotherapeutic *** was capable of inhibiting glycolysis and strengthening endothelial junctions in the human umbilical vein endothelial cells(HUVECs)exposed to ***,SAA was inclined to directly bind to the glycolytic enzyme PKM2,leading to a dramatic decrease in endothelial *** importantly,SAA improved the endothelial integrity via activating theβ-Catenin/Claudin-5 signaling axis in a PKM2-dependent *** findings suggest that SAA may serve as a potent agent for inducing tumor vascular normalization.

关键词： Salvianic acid A Tumor vascular normalization PKM2 β-Catenin Claudin-5 Endothelial glycolysis Tight junctions Doxorubicin

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Microbiome and metabolome dysbiosis analysis in impaired glucose tolerance for the prediction of progression to diabetes mellitus

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Journal of Genetics and Genomics 2024年第1期51卷 75-86页

作者： Boxun Zhang Xuan Zhang Zhen Luo Jixiang Ren Xiaotong Yu Haiyan Zhao Yitian Wang Wenhui Zhang Weiwei Tian Xiuxiu Wei Qiyou Ding Haoyu Yang Zishan Jin Xiaolin Tong Jun Wang Linhua Zhao Institute of Metabolic Diseases Guang'anmen HospitalChina Academy of Chinese Medical SciencesBeijing 100053China Faculty of Biological Science and Technology Baotou Teacher's CollegeBaotouInner Mongolia 014030China CAS Key Laboratory of pathogenic Microbiology and Immunology Institute of MicrobiologyChinese Academy of SciencesBeijing 100101China Infinitus(China)Company Ltd GuangzhouGuangdong 510405China Affiliated Hospital of Changchun University of Chinese Medicine ChangchunJilin 130021China department of Endocrinology Guang'anmen HospitalChina Academy of Chinese Medical SciencesBeijing 100053China Xinjiekou Community Health Service Center in Xicheng District Beijing 100035China department of Spleen and Stomach Shenzhen Traditional Chinese Medicine HospitalShenzhenGuangdong 518033China University of Chinese Academy of Sciences Beijing 100049China Beijing University of Chinese Medicine Beijing 100105China Northeast Asia Institute of Traditional Chinese Medicine Changchun University of Chinese MedicineChangchunJilin 130117China

Gut microbiota and circulating metabolite dysbiosis predate important pathological changes in glucose metabolic disorders;however,comprehensive studies on impaired glucose tolerance(IGT),a diabetes mellitus(DM)precursor,are ***,we perform metagenomic sequencing and metabolomics on 47 pairs of individuals with IGT and newly diagnosed DM and 46 controls with normal glucose tolerance(NGT);patients with IGT are followed up after 4 years for progression to *** of baseline data reveals significant differences in gut microbiota and serum metabolites among the IGT,DM,and NGT *** addition,13 types of gut microbiota and 17 types of circulating metabolites showed significant differences at baseline before IGT progressed to DM,including higher levels of Eggerthella unclassified,Coprobacillus unclassified,Clostridium ramosum,L-valine,L-norleucine,and L-isoleucine,and lower levels of Eubacterium eligens,Bacteroides faecis,Lachnospiraceae bacterium 3_1_46FAA,Alistipes senegalensis,Megaspaera elsdenii,Clostridium perfringens,α-linolenic acid,10E,12Z-octadecadienoic acid,and dodecanoic acid.A random forest model based on differential intestinal microbiota and circulating metabolites can predict the progression from IGT to DM(AUC=0.87).These results suggest that microbiome and metabolome dysbiosis occur in individuals with IGT and have important predictive values and potential for intervention in preventing IGT from progressing to DM.

关键词： Impaired glucose tolerance Diabetes mellitus Gut microbiota Metabolomics

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Non-proteolytic ubiquitination of HBx controls HBV replication

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Virologica Sinica 2024年第2期39卷 338-342页

作者： Xiangpeng Sheng Yi Yang Min Zhu Linlin Zhou Fang Zhu Yuanfei Zhu Siying Dong Hui Kong Honghua Wang Ji Jiang Mingyue Wan Mingyang Feng Qiang Deng Yumin Xu Qing You Ronggui Hu State Key Laboratory for Animal Disease Control and Prevention Harbin Veterinary Research InstituteChinese Academy of Agricultural SciencesHarbin 150069China State Key Laboratory of Molecular Biology Shanghai Institute of Biochemistry and Cell BiologyCenter for Excellence in Molecular Cell ScienceChinese Academy of SciencesShanghai 200031China Key Laboratory of Systems Health Science of Zhejiang Province School of Life ScienceHangzhou Institute for Advanced StudyUniversity of Chinese Academy of SciencesHangzhou 310024China department of Thoracic Surgery Ruijin HospitalShanghai Jiaotong University School of MedicineShanghai 200025China Shanghai Key Laboratory of Plant Molecular Sciences College of Life SciencesShanghai Normal UniversityShanghai 200234China department of pathogenic Biology West China School of Basic Medical Sciences&Forensic MedicineSichuan UniversityChengdu 610041China School of Medicine Guizhou UniversityGuiyang 550025China Key Laboratory of Medical Molecular Virology(MOE&MOH) School of Basic Medical SciencesFudan UniversityShanghai 200032China department of Hospital Infection Management Department of Infectious DiseasesRuijin HospitalShanghai Jiao Tong University School of MedicineShanghai 200025China School of Biomedical Engineering Shanghai Jiao Tong UniversityShanghai 200240China

Dear Editor,Although effective vaccines and antiviral therapies are available,hepatitis B virus(HBV)infection is still a serious global health *** HBV infection remains the principal cause of liver cirrhosis and hepatocellular carcinoma(HCC).HBV is a small DNA virus,owning a~3.2 kb genome that encodes several proteins:viral DNA polymerase,core antigen(HBcAg),E antigen(HBeAg),three surface antigens(PreS1/PreS2/HBsAg),and a regulatory X protein(HBx)(Lamontagne et al.,2016).X protein,named for its lack of homology with any known proteins,is a 154 aa protein that plays an essential role in HBV biology and regulates the development of HCC(Yang et al.,2022).Although previous studies have strongly expanded our understanding of HBx,the regulation of HBx is not completely elucidated.

关键词： infection cirrhosis

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Double-blinded,randomized clinical trial of Gegen Qinlian decoction pinpoints Faecalibacterium as key gut bacteria in alleviating hyperglycemia

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Precision Clinical Medicine 2024年第1期7卷 21-33页

作者： Zezheng Gao Wenhui Zhang Lisha He Han Wang Yufei Li Xiaotian Jiang Sha DI Xinmiao Wang Xuan Zhang Lin Han Yanwen Liu Chengjuan Gu Mengyi Wu Xinhui He Lei Cheng Jun Wang Xiaolin Tong Linhua Zhao Institute of Metabolic Diseases Guang'anmen HospitalChina Academy of Chinese Medical SciencesBeijing 100053China department of Endocrinology Guang anmen HospitalChina Academy of Chinese Medical SciencesBeijing 100053China CAS Key Laboratory of pathogenic Microbiology and Immunology Institute of MicrobiologyChinese Academy of SciencesBeijing 100101China University of Chinese Academy of Sciences Beijing 100049China Chengdu University of Traditional Chinese Medicine Chengdu 611137China School of Chinese Materia Medica Beijing University of Chinese MedicineBeijing 100029China Centre for Evidence-Based Chinese Medicine Beijing University of Chinese MedicineBeijing 100029China department of Endocrinology Affiliated Hospital of Changchun University of Chinese MedicineChangchun 13000oChina Biologicals Science and Technology Institute Baotou Teacher's CollegeBaotou 014030China department of Endocrinology Zhengzhou T.C.M.HospitalZhengzhou 450007China Shenzhen Hospital Guangzhou University of Chinese Medicine(Futian)Shenzhen 518000China department of Cardiology Guangdong Provincial Hospital of Chinese MedicineGuangzhou 510120China department of Cardiology Yunnan Provincial Hospital of Traditional Chinese MedicineKunming 650000China Key Laboratory of Development and Application of Rural Renewable Energy Biogas Institute of Ministry of Agriculture and Rural AffairsChengdu 610041China

Background:Accumulating evidence suggests that metabolic disorders,including type 2 diabetes mellitus(T2DM),can be treated with traditional Chinese medicine formulas,such as the Gegen Qinlian decoction(GQD).This study elucidates the mechanisms by which gut microbes mediate the anti-diabetic effects of ***:We conducted a double-blind randomized clinical trial involving 120 untreated participants with *** the 12-week intervention,anthropometric measurements and diabetic traits were recorded every 4 *** microbiota and serum metabolites were measured before and after the intervention using 16S rDNA sequencing,liquid chromatography-mass spectrometry,and Bio-Plex ***:Anti-diabetic effects were observed in the GQD group in the human ***,glycated hemoglobin,fasting plasma glucose,and two-hour postprandial blood glucose levels were significantly lower in the GQD group than in the placebo ***,Faecalibacterium was significantly enriched in the GQD group,and the short-chain fatty acid levels were higher and the serum inflammation-associated marker levels were lower in the GQD group compared to the placebo ***,Faecalibacterium abundance negatively correlated with the levels of serum hemoglobin,fasting plasma glucose,and pro-inflammatory ***,the diabetes-alleviating effect of Faecalibacterium was confirmed by oral administration of Faecalibacterium prausnitzi(DSMZ 17677)in ***:GQD improved type 2 diabetes primarily by modulating the abundance of Faecalibacterium in the gut microbiota,alleviating metabolic disorders and the inflammatory state.

关键词： double-blinded randomized controlled trial type 2 diabetes mellitus Gegen Qinlian decoction Faecalibacterium metabolic disorders inflammation

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Anti-aquaporin-4 antibody(AQP4-IgG)and anti-myelin oligodendrocyte glycoprotein antibody(MOG-IgG)in the cerebrospinal fluid

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Neural Regeneration Research 2024年第5期19卷 949-950页

作者： Tetsuya Akaishi Tatsuro Misu department of Neurology Tohoku UniversitySendaiJapan

In the last decade,a new neurological disease concept known as anti-myelin oligodendrocyte glycoprotein antibody(MOG-IgG)-associated disease(MOGAD)has emerged and is currently one of the most focused research areas in the field of *** is a membrane protein mainly expressed on the surface of oligodendrocytes(Zhou et al.,2006).The exact pathogenic role of MOG-IgG in patients with MOGAD remains unclear;however,MOG-IgG has been suggested to cause tissue alterations and damage MOG-expressing cells(Zhou et al.,2006).The pathogenicity of MOG-IgG is further supported by the observation that only a few patients with acquired central nervous system(CNS)demyelinating syndromes exhibit both anti-aquaporin-4 antibody(AQP4-IgG)and MOG-IgG simultaneously,particularly with clear positivity levels of these antibodies as indicated by a cell-based assay result with a titer≥1:100(Sechi et al.,2021;Banwell et al.,2023).

关键词： AQP4 myelin

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