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Lupenone improves motor dysfunction in spinal cord injury mice through inhibiting the inflammasome activation and pyroptosis in microglia via the nuclear factor kappa B pathway

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Neural Regeneration Research 2024年第8期19卷 1802-1811页

作者： Fudong Li Xiaofei Sun Kaiqiang Sun Fanqi Kong Xin Jiang Qingjie Kong Department of Orthopedics Shanghai General HospitalShanghai Jiao Tong University School of MedicineShanghaiChina Department of Orthopedic Surgery Spine CenterShanghai Changzheng HospitalNaval Medical UniversityShanghaiChina Department of Orthopedic Surgery Naval Medical CenterNaval Medical UniversityShanghaiChina Department of Anesthesiology Shanghai Changzheng HospitalNaval Medical UniversityShanghaiChina

Spinal cord injury-induced motor dysfunction is associated with neuroinflammation.Studies have shown that the triterpenoid lupenone,a natural product found in various plants,has a remarkable anti-inflammatory effect in the context of chronic inflammation.However,the effects of lupenone on acute inflammation induced by spinal cord injury remain unknown.In this study,we established an impact-induced mouse model of spinal cord injury,and then treated the injured mice with lupenone(8 mg/kg,twice a day)by intrape ritoneal injection.We also treated BV2 cells with lipopolysaccharide and adenosine5’-triphosphate to simulate the inflammatory response after spinal cord injury.Our res ults showed that lupenone reduced IKBa activation and p65 nuclear translocation,inhibited NLRP3 inflammasome function by modulating nuclear factor kappa B,and enhanced the conve rsion of proinflammatory M1 mic roglial cells into anti-inflammatory M2 microglial cells.Furthermore,lupenone decreased NLRP3 inflammasome activation,NLRP3-induced mic roglial cell polarization,and microglia pyroptosis by inhibiting the nuclear factor kappa B pathway.These findings suggest that lupenone protects against spinal cord injury by inhibiting inflammasomes.

关键词： inflammasome inflammation lupenone microglia polarization pyroptosis spinal cord injury

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Tumor necrosis factor-stimulated gene-6 ameliorates early brain injury after subarachnoid hemorrhage by suppressing NLRC4 inflammasome-mediated astrocyte pyroptosis

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Neural Regeneration Research 2024年第5期19卷 1064-1071页

作者： Mingxiang Ding Lei Jin Boyang Wei Wenping Cheng Wenchao Liu Xifeng Li Chuanzhi Duan Neurosurgery Center Department of Cerebrovascular SurgeryThe National Key Clinical SpecialtyThe Engineering Technology Research Center of Education Ministry of China on Diagnosis and Treatment of Cerebrovascular DiseaseGuangdong Provincial Key Laboratory on Brain Function Repair and RegenerationThe Neurosurgery Institute of Guangdong ProvinceZhujiang HospitalSouthern Medical UniversityGuangzhouGuangdong ProvinceChina Department of Cerebrovascular Intervention Zhongshan City People’s HospitalZhongshanGuangdong ProvinceChina

Subarachnoid hemorrhage is associated with high morbidity and mortality and lacks effective treatment.Pyroptosis is a crucial mechanism underlying early brain injury after subarachnoid hemorrhage.Previous studies have confirmed that tumor necrosis factor-stimulated gene-6(TSG-6)can exert a neuroprotective effect by suppressing oxidative stress and apoptosis.However,no study to date has explored whether TSG-6 can alleviate pyroptosis in early brain injury after subarachnoid hemorrhage.In this study,a C57BL/6J mouse model of subarachnoid hemorrhage was established using the endovascular perforation method.Our results indicated that TSG-6 expression was predominantly detected in astrocytes,along with NLRC4 and gasdermin-D(GSDMD).The expression of NLRC4,GSDMD and its N-terminal domain(GSDMD-N),and cleaved caspase-1 was significantly enhanced after subarachnoid hemorrhage and accompanied by brain edema and neurological impairment.To explore how TSG-6 affects pyroptosis during early brain injury after subarachnoid hemorrhage,recombinant human TSG-6 or a siRNA targeting TSG-6 was injected into the cerebral ventricles.Exogenous TSG-6 administration downregulated the expression of NLRC4 and pyroptosis-associated proteins and alleviated brain edema and neurological deficits.Moreover,TSG-6 knockdown further increased the expression of NLRC4,which was accompanied by more severe astrocyte pyroptosis.In summary,our study revealed that TSG-6 provides neuroprotection against early brain injury after subarachnoid hemorrhage by suppressing NLRC4 inflammasome activation-induced astrocyte pyroptosis.

关键词： astrocyte early brain injury inflammasome NLRC4 pyroptosis subarachnoid hemorrhage tumor necrosis factor-stimulated gene-6(TSG-6)

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SLC6A14 promotes ulcerative colitis progression by facilitating NLRP3 inflammasome-mediated pyroptosis

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World Journal of Gastroenterology 2024年第3期30卷 252-267页

作者： Qing Gu Huan Xia Yue-Qiong Song Jun Duan Yun Chen You Zhang He-Ping Chen Li Zhang Department of Elderly Digestive Sichuan Academy of Medical Sciences and Sichuan Provincial People’s HospitalUniversity of Electronic Science and TechnologyChengdu 610072Sichuan ProvinceChina Geriatrics Research Institute Sichuan Provincial People’s HospitalChengdu 610072Sichuan ProvinceChina

BACKGROUND Ulcerative colitis(UC)is an inflammatory condition with frequent relapse and recurrence.Evidence suggests the involvement of SLC6A14 in UC pathogenesis,but the central regulator remains unknown.AIM To explore the role of SLC6A14 in UC-associated pyroptosis.METHODS Quantitative real-time polymerase chain reaction(qRT-PCR),immunoblotting,and immunohistochemical were used to assess SLC6A14 in human UC tissues.Lipopolysaccharide(LPS)was used to induce inflammation in FHC and NCM460 cells and model enteritis,and SLC6A14 levels were assessed.Pyroptosis markers were quantified using enzyme-linked immunosorbent assay,Western blotting,and qRT-PCR,and EdU incubation,CCK-8 assays and flow cytometry were used to examine proliferation and apoptosis.Mouse models of UC were used for verification.RESULTS SLC6A14 was increased and correlated with NLRP3 in UC tissues.LPS-induced FHC and NCM460 cells showed increased SLC6A14 levels.Reducing SLC6A14 increased cell proliferation and suppressed apoptosis.Reducing SLC6A14 decreased pyroptosis-associated proteins(ASC,IL-1β,IL-18,NLRP3).NLRP3 overexpression counteracted the effects of sh-SLC6A14 on LPS-induced FHC and NCM460 cell pyroptosis.SLC6A14 improved the mucosa in mice with dextran sulfate sodium-induced colitis.CONCLUSION SLC6A14 promotes UC pyroptosis by regulating NLRP3,suggesting the therapeutic potential of modulating the SLC6A14/NLRP3 axis.

关键词： Ulcerative colitis SLC6A1 NLRP3 Pyroptosis inflammasome

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Emerging role of exosomes in ulcerative colitis: Targeting NOD-like receptor family pyrin domain containing 3 inflammasome

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World Journal of Gastroenterology 2024年第6期30卷 527-541页

作者： Xin Li Li-Jiang Ji Kai-Di Feng Hua Huang Mei-Rou Liang Shi-Jin Cheng Xiu-Dong Meng School of Basic Medicine Guizhou University of Traditional Chinese MedicineGuiyang 550025Guizhou ProvinceChina Department of Anorectal Surgery Changshu Hospital Affiliated to Nanjing University of Chinese MedicineChangshu 215500Jiangsu ProvinceChina College of Traditional Chinese Medicine Tianjin University of Traditional Chinese MedicineTianjin 301617China

Ulcerative colitis(UC)is a chronic recurrent inflammatory bowel disease.Despite ongoing advances in our understanding of UC,its pathogenesis is yet unelu-cidated,underscoring the urgent need for novel treatment strategies for patients with UC.Exosomes are nanoscale membrane particles that mediate intercellular communication by carrying various bioactive molecules,such as proteins,RNAs,DNA,and metabolites.The NOD-like receptor family pyrin domain containing 3(NLRP3)inflammasome is a cytosolic tripartite protein complex whose activation induces the maturation and secretion of proinflammatory cytokines interleukin-1β(IL-1β)and IL-18,triggering the inflammatory response to a pathogenic agent or injury.Growing evidence suggests that exosomes are new modulators of the NLRP3 inflammasome,with vital roles in the pathological process of UC.Here,recent evidence is reviewed on the role of exosomes and NLRP3 inflammasome in UC.First,the dual role of exosomes on NLRP3 inflammasome and the effect of NLRP3 inflammasome on exosome secretion are summarized.Finally,an outlook on the directions of exosome-NLRP3 inflammasome crosstalk research in the context of UC is proposed and areas of further research on this topic are high-lighted.

关键词： Ulcerative colitis Exosomes inflammasome Evidence Therapeutics

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High glucose reduces Nrf2-dependent cRAGE release and enhances inflammasome-dependent IL-1βproduction in monocytes:the modulatory effects of EGCG

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Food Science and Human Wellness 2024年第3期13卷 1531-1542页

作者： Chi-Hao Wu Yin-Hsuan Chang Chin-Lin Hsu Sheng-Yi Chen Gow-Chin Yen Graduate Programs of Nutrition Science School of Life ScienceTaiwan Normal UniversityTaipei 106209TaiwanChina Department of Food Science and Biotechnology Chung Hsing UniversityTaichung 40227TaiwanChina School of Nutrition Chung Shan Medical UniversityTaichung 40201TaiwanChina

Soluble receptor for advanced glycation end products(sRAGE)acts as a decoy sequestering of RAGE ligands,thus preventing the activation of the ligand-RAGE axis linking human diseases.However,the molecular mechanisms underlying sRAGE remain unclear.In this study,THP-1 monocytes were cultured in normal glucose(NG,5.5 mmol/L)and high glucose(HG,15 mmol/L)to investigate the effects of diabetesrelevant glucose concentrations on sRAGE and interleukin-1β(IL-1β)secretion.The modulatory effects of epigallocatechin gallate(EGCG)in response to HG challenge were also evaluated.HG enhanced intracellular reactive oxygen species(ROS)generation and RAGE expression.The secretion of sRAGE,including esRAGE and cRAGE,was reduced under HG conditions,together with the downregulation of a disintegrin and metallopeptidase 10(ADAM10)and nuclear factor erythroid 2-related factor 2(Nrf2)nuclear translocation.Mechanistically,the HG effects were counteracted by siRAGE and exacerbated by siNrf2.Chromatin immunoprecipitation results showed that Nrf2 binding to the ADAM10 promoter and HG interfered with this binding.Our data reinforce the notion that RAGE and Nrf2 might be sRAGE-regulating factors.Under HG conditions,the treatment of EGCG reduced ROS generation and RAGE activation.EGCG-stimulated cRAGE release was likely caused by the upregulation of the Nrf2-ADAM10 pathway.EGCG inhibited HG-mediated NLRP3 inflammasome activation at least partly by stimulating sRAGE,thereby reducing IL-1βrelease.

关键词： Epigallocatechin gallate(EGCG) inflammasome Nuclear factor erythroid 2-related factor 2(Nrf2) Receptor for advanced glycation end products(RAGE) Soluble RAGE(sRAGE)

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Upregulation of circ0000381 atienuates microglial/macrophage pyroptosis after spinal cord injury

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Neural Regeneration Research 2024年第6期19卷 1360-1366页

作者： Yan Zhang Wenkai Zhang Tao Liu Ziqian Ma Wenxiu Zhang Yun Guan Xueming Chen Central Laboratory Beijing Luhe Hospital Capital Medical University Department of Orthopedics Beijing Luhe Hospital Capital Medical University Department of Emergency Medicine Aerospace Center Hospital Department of Anesthesiology and Critical Care Medicine Johns Hopkins University School of Medicine Department of Neurological Surgery Johns Hopkins University School of Medicine

Neuroinflammation exacerbates secondary damage after spinal cord injury, while microglia/macrophage pyroptosis is important to neuroinflammation. Circular RNAs(circRNAs) play a role in the central nervous system. However, the functional role and mechanism of circRNAs in regulating microglia/macrophage pyroptosis after spinal cord injury are still poorly studied. In the present study, we detected microglia/macrophage pyroptosis in a female rat model of spinal cord injury, along with upregulated levels of circ0000381 in the spinal cord. Our further experimental results suggest that circ0000381 may function as a sponge to sequester endogenous microRNA423-3p(miR-423-3p), which can increase the expression of NOD-like receptor 3(NLRP3), a pyroptosis marker. Therefore, upregulation of circ0000381 may be a compensatory change after spinal cord injury to attenuate microglia/macrophage pyroptosis. Indeed, knockdown of circ0000381 expression exacerbated microglia/macrophage pyroptosis. Collectively, our findings provide novel evidence for the upregulation of circ0000381, which may serve as a neuroprotective mechanism to attenuate microglia/macrophage pyroptosis after spinal cord injury. Accordingly, circ0000381 may be a novel therapeutic target for the treatment of spinal cord injury.

关键词： circ0000381 inflammasome macrophage microglia miR-423-3p neuroinflammation neuroprotection NLRP3 pyroptosis RNA-Seq spinal cord injury

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NLRP3/1-mediated pyroptosis:beneficial clues for the development of novel therapies for Alzheimer’s disease

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Neural Regeneration Research 2024年第11期19卷 2400-2410页

作者： Bo Hu Jiaping Zhang Jie Huang Bairu Luo Xiansi Zeng Jinjing Jia Department of Pathology and Municipal Key-Innovative Discipline of Molecular Diagnostics Jiaxing Hospital of Traditional Chinese MedicineJiaxing UniversityJiaxingZhejiang ProvinceChina Research Center of Neuroscience Jiaxing University Medical CollegeJiaxingZhejiang ProvinceChina Department of Clinical Pathology Jiaxing University Master Degree Cultivation BaseZhejiang Chinese Medical UniversityJiaxingZhejiang ProvinceChina

The inflammasome is a multiprotein complex involved in innate immunity that mediates the inflammatory response leading to pyroptosis,which is a lytic,inflammatory form of cell death.There is accumulating evidence that nucleotide-binding domain and leucine-rich repeat pyrin domain containing 3(NLRP3)inflammasome-mediated microglial pyroptosis and NLRP1 inflammasome-mediated neuronal pyroptosis in the brain are closely associated with the pathogenesis of Alzheimer’s disease.In this review,we summarize the possible pathogenic mechanisms of Alzheimer’s disease,focusing on neuroinflammation.We also describe the structures of NLRP3 and NLRP1 and the role their activation plays in Alzheimer’s disease.Finally,we examine the neuroprotective activity of small-molecule inhibitors,endogenous inhibitor proteins,microRNAs,and natural bioactive molecules that target NLRP3 and NLRP1,based on the rationale that inhibiting NLRP3 and NLRP1 inflammasome-mediated pyroptosis can be an effective therapeutic strategy for Alzheimer’s disease.

关键词： Alzheimer’s disease caspase-1 GSDMD inflammasome neuroinflammation NLRP1 NLRP3 pyroptosis therapeutic strategies

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How location and cellular signaling combine to activate the NLRP3 inflammasome

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Cellular & Molecular Immunology 2022年第11期19卷 1201-1214页

作者： Anil Akbal Alesja Dernst Marta Lovotti Matthew S.J.Mangan Róisín M.McManus Eicke Latz Institute of Innate Immunity University Hospital BonnUniversity of Bonn53127 BonnGermany German Center for Neurodegenerative Diseases 53127 BonnGermany Department of Infectious Diseases&Immunology UMass Medical SchoolWorcesterMA 01605USA Centre of Molecular Inflammation Research Norwegian University of Science and Technology7491 TrondheimNorway

NOD-,LRR-,and pyrin domain-containing 3(NLRP3)is a cytosolic innate immune sensor of cellular stress signals,triggered by infection and sterile inflammation.Upon detection of an activating stimulus,NLRP3 transitions from an inactive homo-oligomeric multimer into an active multimeric inflammasome,which promotes the helical oligomeric assembly of the adaptor molecule ASC.ASC oligomers provide a platform for caspase-1 activation,leading to the proteolytic cleavage and activation of proinflammatory cytokines in the IL-1 family and gasdermin D,which can induce a lytic form of cell death.Recent studies investigating both the cellular requirement for NLRP3 activation and the structure of NLRP3 have revealed the complex regulation of NLRP3 and the multiple steps involved in its activation.This review presents a perspective on the biochemical and cellular processes controlling the assembly of the NLRP3 inflammasome with particular emphasis on structural regulation and the role of organelles.We also highlight the latest research on metabolic control of this inflammatory pathway and discuss promising clinical targets for intervention.

关键词： NLRP3 inflammasome Mechanism Localization Structure Regulation

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USP3 deubiquitinates and stabilizes the adapter protein ASC to regulate inflammasome activation

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Cellular & Molecular Immunology 2022年第10期19卷 1141-1152页

作者： Wanxin Zhuang Lei Zhang Yi Zheng Bingyu Liu Chunhong Ma Wei Zhao Suxia Liu Feng Liu Chengjiang Gao Key Laboratory of Infection and Immunity of Shandong Province&Key Laboratory for Experimental Teratology of Ministry of Education Shandong UniversityJinanShandong250012PR China Department of Immunology School of Biomedical SciencesShandong UniversityJinanShandong250012PR China

inflammasomes are essential components of the innate immune system and its defense against infections,whereas the dysregulation of inflammasome activation has a detrimental effect on human health.The activation of inflammasomes is subjected to tight regulation to maintain immune homeostasis,yet the underlying mechanism remains elusive.Here,we identify USP3 as a direct deubiquitinating enzyme(DUB)for ASC,the central adapter mediating the assembly and activation of most inflammasomes.USP3 removes the K48-linked ubiquitination on ASC and strengthens its stability by blocking proteasomal degradation.Additionally,USP3 promotes inflammasome activation,and this function was confirmed in mouse models of aluminum(Alum)-induced peritonitis,F.novicida infection and flagellin-induced pneumonia in vivo.Our work unveils that USP3 functions as a key regulator of ASC ubiquitination and maintains the physiological role of ASC in mediating inflammasome activation,and we propose a new mechanism by which the ubiquitination of ASC regulates inflammasome activation.

关键词： ASC inflammasome K48-linked ubiquitination proteasomal degradation USP3

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Pnpt1 mediates NLRP3 inflammasome activation by MAVS and metabolic reprogramming in macrophages

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Cellular & Molecular Immunology 2023年第2期20卷 131-142页

作者： Chia George Hsu Wenjia Li Mark Sowden Camila Lage Chávez Bradford C.Berk Department of Medicine Aab Cardiovascular Research InstituteUniversity of RochesterRochesterNYUSA Department of Cardiovascular Medicine Ruijin HospitalShanghai Jiao Tong University School of Medicine200025ShanghaiChina

Polyribonucleotide nucleotidyltransferase 1(Pnpt1)plays critical roles in mitochondrial homeostasis by controlling mitochondrial RNA(mt-RNA)processing,trafficking and degradation.Pnpt1 deficiency results in mitochondrial dysfunction that triggers a type I interferon response,suggesting a role in inflammation.However,the role of Pnpt1 in inflammasome activation remains largely unknown.In this study,we generated myeloid-specific Pnpt1-knockout mice and demonstrated that Pnpt1 depletion enhanced interleukin-1 beta(IL-1β)and interleukin-18(IL-18)secretion in a mouse sepsis model.Using cultured peritoneal and bone marrow-derived macrophages,we demonstrated that Pnpt1 regulated NLRP3 inflammasome-dependent IL-1βrelease in response to lipopolysaccharide(LPS),followed by nigericin,ATP or poly(I:C)treatment.Pnpt1 deficiency in macrophages increased glycolysis after LPS administration and mt-reactive oxygen species(mt-ROS)after NLRP3 inflammasome activation.Pnpt1 activation of the inflammasome was dependent on increased glycolysis and the expression of mitochondrial antiviral-signaling protein(MAVS)but not NF-κB signaling.Collectively,these data suggest that Pnpt1 is an important mediator of inflammation,as shown by activation of the NLRP3 inflammasome in murine sepsis and cultured macrophages.

关键词： Pnpt1 inflammasome Mitochondria Macrophage

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