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Reynosin protects neuronal cells from microglial neuroinflammation by suppressing nlrp3 inflammasome activation mediated by NADPH oxidase

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Chinese Journal of Natural Medicines 2024年第6期22卷 486-500页

作者： YANG Yanqiu CHE Yue FANG Mingxia YAO Xiaohu ZHOU Di WANG Feng CHEN Gang LIANG Dong LI Ning HOU Yue Key Laboratory of Bioresource Research and Development of Liaoning Province College of Life and Health SciencesNorth-eastern UniversityShenyang 110000China National Frontiers Science Center for Industrial Intelligence and Systems Optimization Key Laboratory of Data Analytics and Optimization for Smart IndustryMinistry of EducationNortheastern UniversityShenyang 110000China School of Traditional Chinese Materia Medica Key Laboratory of Innovative Traditional Chinese Medicine for Major Chronic Diseases of Liaoning provinceKey Laboratory for TCM Material Basis Study and Innovative Drug Development of Shenyang CityShenyang Pharmaceutical UniversityShenyang 110000China State Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources School of Chemistry and Pharmaceutical SciencesGuangxi Normal UniversityGuilin 541000China

Neuroinflammation,mediated by the nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing-3(nlrp3)inflammasome,is a significant contributor to the pathogenesis of neurodegenerative diseases(NDDs).Reynos-in,a natural sesquiterpene lactone(SL),exhibits a broad spectrum of pharmacological effects,suggesting its potential therapeutic ***,the effects and mechanism of reynosin on neuroinflammation remain *** current study explores the effects and mechanisms of reynosin on neuroinflammation using mice and BV-2 microglial cells treated with lipopolysaccharide(LPS).Our findings reveal that reynosin effectively reduces microglial inflammation in vitro,as demonstrated by decreased CD11b expression and lowered interleukin-1 beta(IL-1β)and interleukin-18(IL-18)mRNA and protein ***,in vivo,results showed a re-duction in the number of Iba-1 positive cells and alleviation of morphological alterations,alongside decreased expressions of IL-1βand *** analysis indicates that reynosin inhibits nlrp3 inflammasome activation,evidenced by reduced transcription of nlrp3 and caspase-1,diminished nlrp3 protein expression,inhibited apoptosis-associated speck-like protein containing a CARD(ASC)oli-gomerization,and decreased caspase-1 ***,reynosin curtailed the activation of nicotinamide adenine dinuc-leotide phosphate(NADPH)oxidase,demonstrated by reduced NADP^(+)and NADPH levels,downregulation of gp91^(phox) mRNA,pro-tein expression,suppression of p47^(phox) expression and translocation to the ***,reynosin exhibited a neuroprotective effect against microglial inflammation in vivo and in *** collective findings underscore reynosin’s capacity to mitigate mi-croglial inflammation by inhibiting the nlrp3 inflammasome,thus highlighting its potential as a therapeutic agent for managing neuroinflammation.

关键词： Microglia nlrp3 inflammasome Reactive oxygen species NADPH oxidase Neuron Reynosin

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TSPO deficiency exacerbates acute lung injury via nlrp3 inflammasome-mediated pyroptosis

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Chinese Medical Journal 2024年第13期137卷 1592-1602页

作者： Jingyi Han Xue Zhang Menghua Cai Feng Tian Yi Xu Hui Chen Wei He Jianmin Zhang Hui Tian Department of Thoracic Surgery Qilu Hospital of Shandong UniversityJinanShandong 250012China CAMS Key Laboratory of T Cell and Immunotherapy Department of ImmunologyInstitute of Basic Medical SciencesChinese Academy of Medical Sciences and School of Basic MedicinePeking Union Medical CollegeState Key Laboratory of Medical Molecular BiologyBeijing 100005China Changzhou Xitaihu Institute for Frontier Technology of Cell Therapy ChangzhouJiangsu 213000China Haihe Laboratory of Cell Ecosystem Chinese Academy of Medical Sciences&Peking Union Medical CollegeTianjin 300020China

Background:Acute respiratory distress syndrome(ARDS)is a common cause of respiratory failure in many critically ill *** inflammasome activation plays an important role in the induction of acute lung injury(ALI)and ARDS,the regulatory mechanism of this process is still *** cells are stimulated by inflammation,the integrity and physiological function of mitochondria play a crucial part in ***,the underlying mechanisms and function of mitochondrial proteins in the process of pyroptosis are largely not yet ***,we identified the 18-kDa translocator protein(TSPO),a mitochondrial outer membrane protein,as an important mediator regulating nucleotide-binding domain,leucine-rich repeat,and pyrin domain-containing protein 3(nlrp3)inflammasome activation in macrophages during ***:TSPO gene knockout(KO)and lipopolysaccharide(LPS)-induced ALI/ARDS mouse models were employed to investigate the biological role of TSPO in the pathogenesis of *** macrophages were used to further characterize the effect of TSPO on the nlrp3 inflammasome *** of nlrp3 inflammasome was preformed through LPS+adenosine triphosphate(ATP)co-stimulation,followed by detection of mitochondrial membrane potential,reactive oxygen species(ROS)production,and cell death to evaluate the potential biological function of *** between two groups were performed with a two-sided unpaired ***:TSPO-KO mice exhibited more severe pulmonary inflammation in response to LPS-induced *** deficiency resulted in enhanced activation of the nlrp3 inflammasome pathway,promoting more proinflammatory cytokine production of macrophages in LPS-injured lung tissue,including interleukin(IL)-1β,IL-18,and macrophage inflammatory protein(MIP)-*** in TSPO-KO macrophages tended to depolarize in response to cellular *** increased production of mitochondrial damage-associated molecular pattern led to enhanced mitochondrial membr

关键词： Acute respiratory distress syndrome Acute lung injury 18-kDa translocator protein Macrophage nlrp3 inflammasome Inflammation

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An inulin-type fructan CP-A from Codonopsis pilosula attenuates experimental colitis in mice by promoting autophagy-mediated inactivation of nlrp3 inflammasome

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Chinese Journal of Natural Medicines 2024年第3期22卷 249-264页

作者： ZHOU Jiangtao WANG Jun WANG Jiajing LI Deyun HOU Jing LI Jiankuan BAI Yun’e GAO Jianping School of Pharmaceutical Science Shanxi Medical UniversityJinzhong 030600China

Inulin-type fructan CP-A,a predominant polysaccharide in Codonopsis pilosula,demonstrates regulatory effects on immune activity and *** efficacy of CP-A in treating ulcerative colitis(UC)is,however,not *** study employed an in vitro lipopolysaccharide(LPS)-induced colonic epithelial cell model(NCM460)and an in vivo dextran sulfate sodium(DSS)-induced colitis mouse model to explore CP-A’s protective effects against experimental colitis and its underlying *** monitored the clinical symptoms in mice using various parameters:body weight,disease activity index(DAI),colon length,spleen weight,and histopathological ***,molecular markers were assessed through enzyme-linked immunosorbent assay(ELISA),quantitative real-time polymerase chain reaction(qRT-PCR),immunofluorescence(IF),immunohistochemistry(IHC),and Western blotting *** showed that CP-A significantly reduced reactive oxygen species(ROS),tumor necrosis factor-alpha(TNF-α),and interleukins(IL-6,IL-1β,IL-18)in LPS-induced cells while increasing IL-4 and IL-10 levels and enhancing the expression of Claudin-1,ZO-1,and occludin proteins in NCM460 ***,in vivo findings revealed that CPA administration markedly improved DAI,reduced colon shortening,and decreased the production of myeloperoxidase(MPO),malondialdehyde(MDA),ROS,IL-1β,IL-18,and NOD-like receptor protein 3(nlrp3)inflammasome-associated genes/proteins in UC ***-A treatment also elevated glutathione(GSH)and superoxide dismutase(SOD)levels,stimulated autophagy(LC3B,P62,Beclin-1,and ATG5),and reinforced Claudin-1 and ZO-1 expression,thereby aiding in intestinal epithelial barrier repair in colitis ***,the inhibition of autophagy via chloroquine(CQ)diminished CP-A’s protective impact against colitis in *** findings elucidate that CP-A’s therapeutic effect on experimental colitis possibly involves mitigating intestinal inflammation through autophagymediated N

关键词： Inulin-type fructan CP-A Codonopsis pilosula Ulcerative colitis nlrp3 inflammasome Autophagy

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Endoplasmic reticulum stress-induced nlrp3 inflammasome activation as a novel mechanism of polystyrene microplastics (PS-MPs)-induced pulmonary inflammation in chickens

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Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2024年第3期25卷 233-243页

作者： Hongmin LU Tiantian GUO Yue ZHANG Dewang LIU Lulu HOU Chengxue MA Mingwei XING College of Wildlife and Protected Area Northeast Forestry UniversityHarbin 150040China

Microplastics(MPs)have attracted growing attention worldwide as an increasingly prevalent environmental *** addition,chicken meat is currently the most widely consumed kind of poultry in the global *** demand for chicken is on the rise both at home and *** a result,the safety of chicken raising has also received significant *** lungs play an essential role in the physiological activities of chickens,and they are also the most vulnerable *** injury is difficult to repair after the accumulation of contaminants,and the mortality rate is high,which brings huge economic losses to *** research on the toxicity of MPs has mainly focused on the marine ecosystem,while the mechanisms of toxicity and lung damage in chickens have been poorly ***,this study explored the effects of exposure to polystyrene microplastics(PS-MPs)at various concentrations for 42 d on chicken ***-MPs could cause lung pathologies and ultrastructural abnormalities,such as endoplasmic reticulum(ER)swelling,inflammatory cell infiltration,chromatin agglutination,and plasma membrane ***,PS-MPs increased the expression of genes related to the heat shock protein family(Hsp60,Hsp70,and Hsp90),ER stress signaling(activating) transcription factor 6(ATF0),ATF4,protein kinase RNA-like ER kinase(PERK),and eukaryotic translation initiation factor 2 subunitα(eIF2a),pyroptosis-related genes(NOD)-,LRR-and pyrin domain-containing protein 3(nlrp3),apoptosis-associated speck-like protein containing a caspase recruitment domain(ASC),interleukin-1β(IL-1β),cysteinyl aspartate-specific proteinase 1(Caspasel),and gasdermin-D(GSDMD),and the inflammatory signaling pathway(nuclear factor-kB(NF-kB),inducible nitric oxide synthase(iNOS),and cyclooxygenase-2(COX-2).The above results showed that PS-MP exposure could result in lung stress,ER stress,pyroptosis,and inflammation in *** findings provide new scientific clues for further research o

关键词： Polystyrene microplastics Endoplasmic reticulum stress Lung nlrp3 inflammasome Inflammation

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Paeoniflorin alleviates depression by inhibiting the activation of nlrp3 inflammasome via promoting mitochondrial autophagy

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Chinese Journal of Natural Medicines 2024年第6期22卷 515-529页

作者： SU Lili GUO Pengli GUO Xiangjuan HE Zhongmei ZHAO Yan ZONG Ying LI Jianming CHEN Weijia DU Rui College of Chinese Medicinal Materials Jilin Agricultural UniversityChangchun 130118China Jilin Provincial Engineering Research Center for Efficient Breeding and Product Development of Sika Deer Changchun 130118China Key Laboratory of Animal Production and Product Quality and Security Ministry of EducationMinistry of National EducationChangchun 130118China

Depression ranks among the most common neuropsychiatric disorders *** studies examining the roles of inflammation and mitochondrial autophagy in the antidepressant efficacy of paeoniflorin(PF)are *** study aimed to elucidate PF’s antidepressant mechanism by promoting autophagy and inhibiting nlrp3 inflammasome activation using chronic unpredictable mild stimulation(CUMS)-induced C57BL/6 mouse models in vivo and corticosterone(CORT)-induced HT22 cell models in *** demonstrated that PF enhanced the viability of HT22 cells following CORT exposure,restored mitochondrial membrane poten-tial(MMP),reduced reactive oxygen species accumulation,increased LC3 fluorescence intensity,and suppressed inflammatory cy-tokine secretion and inflammation ***,PF ameliorated depressive behaviors induced by CUMS and improved damage in hippocampal *** also reduced the expression of nlrp3,ASC,Caspase-1,IL-1β,and the assembly of the nlrp3 ***,PF upregulated the expression of autophagy-related proteins in the hippocampus,facilitating the clearance of damaged mitochondria and enhancing *** role of autophagy in PF’s antidepressant effects was further confirmed through the use of the autophagy inhibitor 3-methyladenine(3-MA),which reduced the efficacy of *** conclusion,PF effectively improved depressive behaviors in CUMS-induced mice and reduced nlrp3-mediated inflammation both in vivo and in vitro,likely via the in-duction of autophagy.

关键词： Paeoniflorin Depression Autophagy nlrp3 inflammasome

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Fantastic voyage: The journey of nlrp3 inflammasome activation

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Genes & Diseases 2024年第2期11卷 819-829页

作者： Xiangyong Que Sihao Zheng Qibin Song Huadong Pei Pingfeng Zhang Cancer Center Renmin Hospital of Wuhan UniversityWuhanHubei 430060China Department of Oncology Georgetown Lombardi Comprehensive Cancer CenterGeorgetown University Medical CenterWashingtonDC 20057USA

nlrp3 inflammasome,an intracellular multiprotein complex,can be activated by a range of pathogenic microbes or endogenous hazardous *** activation results in the release of cytokines such as IL-1β and IL-18,as well as Gasdermin D which eventually causes *** activation of nlrp3 inflammasome is under strict control and regulation by numerous pathways and *** excessive activation can lead to a persistent inflammatory response,which is linked to the onset and progression of severe *** studies have revealed that the subcellular localization of nlrp3 changes significantly during the activation *** this review,we review the current understanding of the molecular mechanism of nlrp3 inflammasome activation,focusing on the subcellular localization of nlrp3 and the associated regulatory *** aim to provide a comprehensive understanding of the dynamic transportation,activation,and degradation processes of nlrp3.

关键词： inflammasome activation Innate immunity nlrp3 nlrp3 inflammasome Subcellular localization

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Microglial nlrp3 inflammasome-mediated neuroinflammation and therapeutic strategies in depression

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Neural Regeneration Research 2024年第9期19卷 1890-1898页

作者： Qiuqin Han Wenhui Li Peiqing Chen Lijuan Wang Xiwen Bao Renyan Huang Guobin Liu Xiaorong Chen Department of Scientific Research Shanghai University of Medicine&Health Sciences Affiliated Zhoupu HospitalShanghaiChina Department of Traditional Chinese Vascular Surgery Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese MedicineShanghaiChina Department of Physiology Laboratory of Neurodegenerative DiseasesChangzhi Medical CollegeChangzhiShanxi ProvinceChina

Previous studies have demonstrated a bidirectional relationship between inflammation and *** of the nucleotide-binding oligomerization domain,leucine-rich repeat,and NLR family pyrin domain-containing 3(nlrp3)inflammasomes is closely related to the pathogenesis of various neurological *** patients with major depressive disorder,nlrp3 inflammasome levels are significantly *** the role that nlrp3 inflammasome-mediated neuroinflammation plays in the pathogenesis of depression may be beneficial for future therapeutic *** this review,we aimed to elucidate the mechanisms that lead to the activation of the nlrp3 inflammasome in depression as well as to provide insight into therapeutic strategies that target the nlrp3 ***,we outlined various therapeutic strategies that target the nlrp3 inflammasome,including nlrp3 inflammatory pathway inhibitors,natural compounds,and other therapeutic compounds that have been shown to be effective in treating ***,we summarized the application of nlrp3 inflammasome inhibitors in clinical trials related to ***,there is a scarcity of clinical trials dedicated to investigating the applications of nlrp3 inflammasome inhibitors in depression *** modulation of nlrp3 inflammasomes in microglia holds promise for the management of *** investigations are necessary to ascertain the efficacy and safety of these therapeutic approaches as potential novel antidepressant treatments.

关键词： depression microglia neuroinflammation nlrp3 inflammasome

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Elaidic acid-induced intestinal barrier damage led to gut-liver axis derangement and triggered nlrp3 inflammasome in the liver of SD rats

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Food Science and Human Wellness 2024年第3期13卷 1279-1291页

作者： Hui Liu Xuenan Li Lu Li Yucai Li Haiyang Yan Yong Pang Wenliang Li Yuan Yuan College of Food Science and Engineering Jilin UniversityChangchun 130062China School of Public Health Jining Medical UniversityJining 272067China

Previous studies have shown that trans fatty acids(TFA) are associated with several chronic diseases,the gut microbiota is directly influenced by dietary components and linked to chronic *** research investigated the effects of elaidic acid(EA),a typical TFA,on the gut microbiota to understand the underlying mechanisms of TFA-related chronic diseases.16S rDNA gene sequencing on faecal samples from Sprague-Dawley rats were performed to explore the composition change of the gut microbiota by EA gavage for 4 *** results showed that the intake of EA increased the abundance of well-documented harmful bacteria,such as Proteobacteria,Anaerotruncus,Oscillibacter and ***,EA induced translocation of lipopolysaccharides(LPS) and the above pathogenic bacteria,disrupted the intestinal barrier,led to gut-liver axis derangement and TLR4 pathway activation in the ***,EA induced intestinal barrier damage and regulated TLR4-MyD88-NF-κB/MAPK pathways in the liver of SD rats,leading to the activation of nlrp3 inflammasome and inflammatory liver damage.

关键词： Elaidic acid(EA) Gut microbiota Intestinal barrier Gut-liver axis TLR4-MyD88-NF-κB/MAPK pathways nlrp3 inflammasome

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Repurposing disulfiram with CuET nanocrystals:Enhancing anti-pyroptotic effect through nlrp3 inflammasome inhibition for treating inflammatory bowel diseases

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Acta Pharmaceutica Sinica B 2024年第6期14卷 2698-2715页

作者： Xueming Xu Yuanfeng Han Jiali Deng Shengfeng Wang Shijie Zhuo Kai Zhao Wenhu Zhou Hematology and Department of Critical Care Medicine The Third Xiangya HospitalCentral South UniversityChangsha 410013China Xiangya School of Pharmaceutical Sciences Central South UniversityChangsha 410013China Hunan Chidren's Hospital Changsha 410007China Department of Pharmacy The Third Xiangya HospitalCentral South UniversityChangsha 410013China Key Laboratory of Biological Nanotechnology of National Health Commission Changsha 410008China

Drug repurposing offers a valuable strategy for identifying new therapeutic applications for existing ***,disulfiram(DSF),a drug primarily used for alcohol addiction treatment,has emerged as a potential treatment for inflammatory diseases by inhibiting pyroptosis,a form of programmed cell *** therapeutic activity of DSF can be further enhanced by the presence of Cu^(2+),although the underlying mechanism of this enhancement remains *** this study,we investigated the mechanistic basis of Cu^(2+)-induced enhancement and discovered that it is attributed to the formation of a novel copper ethylthiocarbamate(CuET)*** exhibited significantly stronger anti-pyroptotic activity compared to DSF and employed a distinct mechanism of ***,despite its potent activity,CuET suffered from poor solubility and limited permeability,as revealed by our druggability *** overcome these intrinsic limitations,we developed a scalable method to prepare CuET nanocrystals(CuET NCs)using a metal coordination-driven self-assembly *** studies demonstrated that CuET NCs exhibited a 6-fold improvement in ***,CuET NCs exhibited high biodistribution in the intestine,suggesting their potential application for the treatment of inflammatory bowel diseases(IBDs).To evaluate their therapeutic efficacy in vivo,we employed a murine model of DSS-induced colitis and observed that CuET NCs effectively attenuated inflammation and ameliorated colitis *** findings highlight the discovery of CuET as a potent anti-pyroptotic agent,and the development of CuET NCs represents a novel approach to enhance the druggability of CuET.

关键词： Drug repurposing Pyroptosis Nanoparticles Bioavailability Disulfiram DSS-induced colitis nlrp3 inflammasome CuET

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Nuclear receptor coactivator 6 is a critical regulator of nlrp3 inflammasome activation and gouty arthritis

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Cellular & Molecular Immunology 2024年第3期21卷 227-244页

作者： Kang-Gu Lee Bong-Ki Hong Saseong Lee Naeun Lee Seung-Whan Kim Donghyun Kim Wan-Uk Kim Center for Integrative Rheumatoid Transcriptomics and Dynamics The Catholic University of KoreaSeoul 06591Republic of Korea Department of Biomedicine&Health Sciences The Catholic University of KoreaSeoul 06591Republic of Korea Department of Pharmacology Asan Medical CenterUniversity of Ulsan College of MedicineSeoul 05505Republic of Korea Bio-Medical Institute of Technology University of UlsanSeoul 05505Republic of Korea Department of Microbiology and Immunology Seoul National University College of MedicineSeoul 03080Republic of Korea Institute of Infectious Diseases Seoul National University College of MedicineSeoul 03080Republic of Korea Division of Rheumatology Department of Internal MedicineThe Catholic University of KoreaSeoul 06591Republic of Korea

Transcriptional coactivators regulate the rate of gene expression in the *** receptor coactivator 6(NCOA6),a coactivator,has been implicated in embryonic development,metabolism,and cancer pathogenesis,but its role in innate immunity and inflammatory diseases remains ***,we demonstrated that NCOA6 was expressed in monocytes and macrophages and that its level was increased under proinflammatory ***,nuclear NCOA6 was found to translocate to the cytoplasm in activated monocytes and then become incorporated into the inflammasome with nlrp3 and ASC,forming cytoplasmic ***,NCOA6 associated with the ATP hydrolysis motifs in the NACHT domain of nlrp3,promoting the oligomerization of nlrp3 and ASC and thereby instigating the production of IL-1βand active *** note,Ncoa6 deficiency markedly inhibited nlrp3 hyperactivation caused by the nlrp3^(R258W) gain-of-function mutation in *** ablation of Ncoa6 substantially attenuated the severity of two nlrp3-dependent diseases,folic-induced acute tubular necrosis and crystal-induced arthritis,in *** with these findings,NCOA6 was highly expressed in macrophages derived from gout patients,and NCOA6-positive macrophages were significantly enriched in gout macrophages according to the transcriptome profiling ***,NCOA6 is a critical regulator of nlrp3 inflammasome activation and is therefore a promising target for nlrp3-dependent diseases,including gout.

关键词： Nuclear receptor coactivator 6 Nuclear-to-cytoplasmic translocation nlrp3 inflammasome NACHT domain Gouty arthritis

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