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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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WNT/β-catenin signaling in hepatocellular carcinoma:The aberrant activation,pathogenic roles,and therapeutic opportunities

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Genes & Diseases 2024年第2期11卷 727-746页

作者： Anna Gajos-Michniewicz Malgorzata Czyz department of Molecular biology of Cancer Medical University of LodzLodz 92-215Poland

Hepatocellular carcinoma(HCC)is a liver cancer,highly heterogeneous both at the histopathological and molecular *** arises from hepatocytes as the result of the accumulation of numerous genomic alterations in various signaling pathways,including canonical WNT/β-catenin,AKT/mTOR,MAPK pathways as well as signaling associated with telomere maintenance,p53/cell cycle regulation,epigenetic modifiers,and oxidative *** role of WNT/β-catenin signaling in liver homeostasis and regeneration is well established,whereas in development and progression of HCC is extensively ***,we review recent advances in our understanding of how WNT/β-catenin signaling facilitates the HCC development,acquisition of stemness features,metastasis,and resistance to *** outline genetic and epigenetic alterations that lead to activated WNT/β-catenin signaling in *** discuss the pivotal roles of CTNNB1 mutations,aberrantly expressed non-coding RNAs and complexity of crosstalk between WNT/β-catenin signaling and other signaling pathways as challenging or advantageous aspects of therapy development and molecular stratification of HCC patients for treatment.

关键词： Cancer stem cells CTNNB1 mutations Liver cancer Non-coding RNA Tumor heterogeneity

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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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Cmtm4 deficiency exacerbates colitis by inducing gut dysbiosis and S100a8/9 expression

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Journal of Genetics and Genomics 2024年第8期51卷 811-823页

作者： Qiao Meng Jing Ning Jingjing Lu Jing Zhang Ming Zu Jing Zhang Xiurui Han Huiling Zheng Yueqing Gong Xinyu Hao Ying Xiong Fang Gu Wenling Han Weiwei Fu Jun Wang Shigang Ding department of Gastroenterology Peking University Third HospitalBeijing 100191China Beijing Key Laboratory for Helicobacter Pylori Infection and Upper Gastrointestinal Diseases(BZ0371) Beijing 100191China CAS Key Laboratory of pathogenic Microbiology and Immunology Institute of MicrobiologyChinese Academy of SciencesBeijing 100101China University of Chinese Academy of Sciences Beijing 100101China department of Immunology School of Basic Medical SciencesPeking University Health Science CenterNHC Key Laboratory of Medical Immunology(Peking University)Beijing 100191China Peking University Center for Human Disease Genomics Beijing 100191China

The dysfunction of innate immunity components is one of the major drivers for ulcerative colitis(UC),and increasing reports indicate that the gut microbiome serves as an intermediate between genetic mutations and UC ***,we find that the IL-17 receptor subunit,CMTM4,is reduced in UC patients and dextran sulfate sodium(DSS)-induced *** deletion of CMTM4(Cmtm4^(-/-))in mice leads to a higher susceptibility to DSS-induced colitis than in wild-type,and the gut microbiome significantly changes in *** causal role of the gut microbiome is confirmed with a cohousing *** further identify that S100a8/9 is significantly up-regulated in Cmtm4^(-/-)colitis,with the block of its receptor RAGE that reverses the phenotype associated with the CMTM4 ***4 deficiency rather suppresses S100a8/9 expression in vitro via the IL17 pathway,further supporting that the elevation of S100a8/9 in vivo is most likely a result of microbial *** together,the results suggest that CMTM4 is involved in the maintenance of intestinal homeostasis,suppression of S100a8/9,and prevention of colitis *** study further shows CMTM4 as a crucial innate immunity component,confirming its important role in UC development and providing insights into potential targets for the development of future therapies.

关键词： Ulcerative colitis CMTM4 Gut microbiota IL-17 receptor C(IL-17RC) S100a8/9

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Visible light cross-linking and bioactive peptides loaded integrated hydrogel with sequential release to accelerate wound healing complicated by bacterial infection

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Nano Research 2024年第3期17卷 1737-1747页

作者： Guiyan Wang Ning Yuan Jun Zhang Man Qin Suwei Dong Yuguang Wang department of Pediatric Dentistry Peking University School and Hospital of StomatologyBeijing 100081China State Key Laboratory of Natural and Biomimetic Drugs Chemical Biology Centerand School of Pharmaceutical SciencesPeking UniversityBeijing 100191China department of Prosthodontics Peking University School and Hospital of StomatologyBeijing 100081China

The effective management of bacterial infections that are resistant to multiple drugs remains a substantial clinical *** eradication of drug-resistant bacteria and subsequent promotion of angiogenesis are imperative for the regeneration of the infected ***,a novel and facile peptide containing injectable hydrogel with sustained antibacterial and angiogenic capabilities is *** antibacterial peptide that consists of 11 residues(CM11,WKLFKKILKVL)is loaded onto acrylate-modified gelatin through charge interactions.A vascular endothelial growth factor mimetic peptide KLT(KLTWQELYQLKYKGI)with a GCG(Gly-Cys-Gly)modification at the N-terminal is covalently coupled through a visible light-induced thiol-ene *** this reaction,the acrylate gelatin undergoes cross-linkage within *** on the physical/chemical double crosslinking strategy,the bioactive peptides achieve sustained and sequential *** results show that the hydrogel significantly inhibits methicillin-resistant Staphylococcus aureus(MRSA)growth through the rapid release of CM11 peptides at early stage;it forms obvious growth inhibition zones against pathogenic bacterial ***,cell counting kit-8 assay and scratch test confirm that the CM11/KLT-functionalized hydrogels promote cell proliferation and migration through the later release of KLT *** a mouse skin wound infected with self-luminous MRSA,the CM11/KLT-functionalized hydrogels enhance wound healing,with rapidly bacterial infection reduction,lower expression of inflammatory factors,and neovascularization *** results suggest that the rationally designed,sustained and sequential release CM11/KLT-functionalized hydrogels have huge potential in promoting the healing of multi-drug resistant bacterial infected wounds.

关键词： antimicrobial peptide vascular endothelial growth factor(VEGF)mimetic peptide sequential release visible-light crosslinking hydrogel wound therapy

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Hordedane diterpenoid phytoalexins restrict Fusarium graminearum infection but enhance Bipolaris sorokiniana colonization of barley roots

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Molecular Plant 2024年第8期17卷 1307-1327页

作者： Yaming Liu Dario Esposto Lisa K.Mahdi Andrea Porzel Pauline Stark Hidayat Hussain Anja Scherr-Henning Simon Isfort Ulschan.Bathe Ivan F.Acosta Alga Zuccaro Gerd U.Balcke Alain Tissier department of Cell and Metabolic biology Leibniz Institute of Plant BiochemistryHalleGermany institute for Plant Sciences Cluster of Excellence on Plant Sciences(CEPLAS)Cologne BiocenterUniversity of CologneCologneGermany department of Bioorganic Chemistry Leibniz Institute of Plant BiochemistryHalleGermany Max Planck Institute for Plant Breeding Research CologneGermany Horticultural Sciences University of FloridaGainesvilleFLUSA.

Plant immunity is a multilayered process that includes recognition of patterns or effectors from pathogens to elicit defense *** include the induction of a cocktail of defense metabolites that typically restrict pathogen ***,we investigate the interaction between barley roots and the fungal pathogens Bipolaris sorokiniana(Bs)and Fusarium graminearum(Fg)at the metabolite *** identify hordedanes,a previously undescribed set of labdane-related diterpenoids with antimicrobial properties,as critical players in these *** of barley roots by Bs and Fg elicits hordedane synthesis from a 60o-kb gene *** reconstruction of the biosynthesis pathway in yeast and Nicotiana benthamiana produced several hordedanes,including one of the most functionally decorated products 19-β-hydroxy-hordetrienoic acid(19-OH-HTA).Barley mutants in the diterpene synthase genes of this cluster are unable to produce hordedanes but,unexpectedly,show reduced Bs *** contrast,colonization by Fusarium graminearum,another fungal pathogen of barley and wheat,is 4-fold higher in the mutants completely lacking ***,19-OH-HTA enhances both germination and growth of Bs,whereas it inhibits other pathogenic fungi,including *** of microscopy and transcriptomics data suggest that hordedanes delay the necrotrophic phase of *** together,these results show that adapted pathogens such as Bs can subvert plant metabolic defenses to facilitate root colonization.

关键词： barley Hordeum vulgare diterpenoid phytoalexins gene cluster pathogenic fungi Bipolaris sorokininiana Fusarium graminearum

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E674Q(Shanghai APP mutant),a novel amyloid precursor protein mutation,in familial late-onset Alzheimer's disease

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Genes & Diseases 2024年第2期11卷 1022-1034页

作者： Yongfang Zhang Xinyi Xie Boyu Chen Lina Pan Jianping Li Wanbing Wang Jintao Wang Ran Tang Qiang Huang Xiaofen Chen Rujing Ren Zhentao Zhang Wei Fu Gang Wang department of Neurology Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of MedicineShanghai 200025China department of Pharmacology and Chemical biology Shanghai Jiao Tong University School of MedicineShanghai 200025China department of Medicinal Chemistry School of PharmacyFudan UniversityShanghai 201203China department of Neurology Renmin Hospital of Wuhan UniversityWuhanHubei 430060China Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research Institute of NeuroscienceSchool of MedicineXiamen UniversityXiamenFujian 361102China Shenzhen Research Institute of Xiamen University ShenzhenGuangdong 518063China

Identified as the pathogenic genes of Alzheimer's disease(AD),APP,PSEN1,and PSEN2 mainly lead to early-onset AD,whose course is more aggressive,and atypical symptoms are more common than sporadic ***,a novel missense mutation,APP E674Q(also named“Shanghai APP”),was detected in a Chinese index patient with typical late-onset AD(LOAD)who developed memory decline in his *** results from neuroimaging were consistent with AD,where widespread amyloidβdeposition was demonstrated in 18 F-florbetapir Positron Emission Tomography(PET).APP E674Q is close to theβ-secretase cleavage site and the well-studied Swedish APP mutation(KM670/671NL),which was predicted to be pathogenic in *** dynamics simulation indicated that the E674Q mutation resulted in a rearrangement of the interaction mode between APP and BACE1 and that the E674Q mutation was more prone to cleavage by *** in vitro results suggested that the E674Q mutation was pathogenic by facilitating the BACE1-mediated processing of APP and the production of Aβ.Furthermore,we applied an adeno-associated virus(AAV)-mediated transfer of the human E674Q mutant APP gene to the hippocampi of two-month-old C57Bl/6 J ***-E674Q-injected mice exhibited impaired learning behavior and increased pathological burden in the brain,implying that the E674Q mutation had a pathogenicity that bore a comparison with the classical Swedish ***,we report a strong amyloidogenic effect of the E674Q substitution in *** our knowledge,E674Q is the only pathogenic mutation within the amyloid processing sequence causing LOAD.

关键词： Alzheimer's disease Amyloid beta APP mutation E674Q Late onset

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Fungi Associated with Sand and Plants from Marine Coastlines: Potential Relevance for Human Health

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Advances in Microbiology 2024年第6期14卷 303-316页

作者： Marina Carrasco-Acosta Pilar Garcia-Jimenez department of biology Universidad de Las Palmas de Gran Canaria Campus de Tafira Las Palmas Spain

The fungal community associated with beach sand and plants located along marine coasts are an under-studied area of research despite its potential relevance to human health. In this study, we isolated and identified the cultivable mycobiota associated with sand and plants collected along the coast of Gran Canaria (Spain) using culture-dependent and -independent methods. Clinically relevant species belonging to Cryptococcus spp. and related genera such as Naganishia and Papilotrema were isolated and identified from shoreline plants. Moreover, Candida tropicalis was isolated from beach sand, and Aspergillus fumigatus and Aspergillus terreus strains were associated with both types of samples (i.e., plants and beach sand). We conclude that beach sand and shoreline plants are potential reservoirs of fungi of high clinical interest. We recommend including beach sand and plants from the environment when assessing the quality of marine coastal systems. Our results open a framework for studying the natural marine environment and its role in the epidemiology of infectious diseases in order to more accurately manage public health.

关键词： Sand Beach Shoreline Plants Reservoir of pathogenic Fungi Cryptococcus spp. Aspergillus spp.

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Therapeutic targeting of cellular prion protein: toward the development of dual mechanism anti-prion compounds

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Neural Regeneration Research 2025年第4期20卷 1009-1014页

作者： Antonio Masone Chiara Zucchelli Enrico Caruso Giovanna Musco Roberto Chiesa Laboratory of Prion Neurobiology Department of NeuroscienceIstituto di Ricerche Farmacologiche Mario Negri IRCCSMilanItaly Biomolecular NMR Unit Division of Genetics and Cell BiologyIRCCS Ospedale San RaffaeleMilanItaly department of Biotechnology and Life Sciences University of InsubriaVareseItaly

PrPSc,a misfolded,aggregation-prone isoform of the cellular prion protein(PrPC),is the infectious prion agent responsible for fatal neurodegenerative diseases of humans and other *** adopt different pathogenic conformations(prion strains),which can be resistant to potential drugs,or acquire drug resistance,posing challenges for the development of effective *** PrPCis the obligate precursor of any prion strain and serves as the mediator of prion neurotoxicity,it represents an attractive therapeutic target fo r prion *** this minireview,we briefly outline the approaches to target PrPCand discuss our recent identification of Zn(Ⅱ)-Bn PyP,a PrPC-targeting porphyrin with an unprecedented bimodal mechanism of *** argue that in-depth understanding of the molecular mechanism by which Zn(Ⅱ)-Bn PyP targets PrPCmay lead toward the development of a new class of dual mechanism anti-prion compounds.

关键词： anti-prion drug anti-PrPC antibody antisense oligonucleotide neurodegeneration pharmacological chaperone porphyrin prion disease PrPC degrader PrPC shedding zinc finger repressor

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