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Journal of Pharmaceutical Analysis 2023年第9期13卷 999-1012页

作者： Jian Zou Rujie Yang Ruibing Feng Jiayue Liu Jian-Bo Wan State Key Laboratory of Quality Research in Chinese Medicine Institute of Chinese Medical SciencesUniversity of MacaoMacao SARChina

Heavy alcohol consumption results in alcoholic liver disease(ALD)with inadequate therapeutic ***,we first report the potential beneficial effects of ginsenoside Rk2(Rk2),a rare dehydroprotopanaxadiol saponin isolated from streamed ginseng,against alcoholic liver injury in ***-plus-single-binge ethanol feeding caused severe liver injury,as manifested by significantly elevated serum aminotransferase levels,hepatic histological changes,increased lipid accumulation,oxidative stress,and inflammation in the *** deleterious effects were alleviated by the treatment with Rk2(5 and 30 mg/kg).Acting as an nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3(nlrp3)inhibitor,Rk2 ameliorates alcohol-induced liver inflammation by inhibiting nlrp3 inflammasome signaling in the ***,the treatment with Rk2 alleviated the alcohol-induced intestinal barrier dysfunction via enhancing nlrp6 inflammasome in the *** findings indicate that Rk2 is a promising agent for the prevention and treatment of ALD and other NLPR3-driven diseases.

关键词： Alcoholic liver disease Ginsenoside Rk2 nlrp3 inflammasome nlrp6 inflammasome Intestinal barrier dysfunction

Dual‑Atom Nanozyme Eye Drops Attenuate Inflammation and Break the Vicious Cycle in Dry Eye Disease

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Nano-Micro Letters 2024年第6期16卷 439-457页

作者： Dandan Chu Mengyang Zhao Shisong Rong Wonho Jhe Xiaolu Cai Yi Xiao Wei Zhang Xingchen Geng Zhanrong Li Xingcai Zhang Jingguo Li Henan Eye Hospital Henan Provincial People’s HospitalPeople’s Hospital of Zhengzhou UniversityZhengzhou 450003People’s Republic of China Department of Ophthalmology Mass Eye and EarMass General BrighamHarvard Medical SchoolBostonMA 02114USA School of Engineering and Applied Sciences Harvard UniversityCambridgeMA 02138USA College of Chemistry Zhengzhou UniversityZhengzhou 450001People’s Republic of China

Dry eye disease(DED)is a major ocular pathology worldwide,causing serious ocular discomfort and even visual *** incidence of DED is gradually increasing with the highfrequency use of electronic *** inflammation is core cause of the DED vicious cycle,reactive oxygen species(ROS)play a pivotal role in the vicious cycle by regulating inflammation from ***,current therapies merely targeting inflammation show the failure of DED ***,a novel dual-atom nanozymes(DAN)-based eye drops are *** antioxidative DAN is successfully prepared by embedding Fe and Mn bimetallic single-atoms in N-doped carbon material and modifying it with a hydrophilic *** in vitro and in vivo results demonstrate the DAN is endowed with superior biological activity in scavenging excessive ROS,inhibiting nlrp3 inflammasome activation,decreasing proinflammatory cytokines expression,and suppressing cell ***,the DAN effectively alleviate ocular inflammation,promote corneal epithelial repair,recover goblet cell density and tear secretion,thus breaking the DED vicious *** findings open an avenue to make the DAN as an intervention form to DED and ROSmediated inflammatory diseases.

关键词： Dry eye disease DAN Dual-atom nanozyme Vicious cycle nlrp3 inflammasome Nanomedicine

Yanggan Jiangmei Formula alleviates hepatic inflammation and lipid accumulation in non-alcoholic steatohepatitis by inhibiting the NF-κB/nlrp3 signaling pathway

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Chinese Journal of Natural Medicines 2024年第3期22卷 224-234页

作者： WU Yuanyuan ZHOU Jingwen ZUO Xinchen KUANG Yufeng SUN Lixia ZHANG Xiaolong The First Clinical Medical College Nanjing University of Chinese MedicineNanjing 210023China The Affiliated Hospital of Nanjing University of Chinese Medicine Jiangsu Province Hospital of Chinese MedicineNanjing 210029China

The role of NF-κB and the nlrp3 inflammasome in the chronic inflammatory microenvironment of non-alcoholic steatohepatitis(NASH)has been posited as *** Yanggan Jiangmei Formula(YGJMF)has shown promise in ameliorating hepatic steatosis in NASH patients,yet its pharmacological mechanisms remain largely *** study was conducted to investigate the efficacy of YGJMF in NASH and to elucidate its pharmacological *** simulate NASH both in vivo and in vitro,high-fat-diet(HFD)rats and HepG2 cells stimulated with free fatty acids(FFAs)were *** severity of liver injury and lipid deposition was assessed using serum indicators,histopathological staining,micro-magnetic resonance imaging(MRI),and the liver-tomuscle signal intensity ratio(SIRL/M).Furthermore,a combination of enzyme-linked immunosorbent assay(ELISA),immunohistochemistry(IHC),immunofluorescence,real-time quantitative polymerase chain reaction(RT-qPCR),and Western blotting analyses was employed to investigate the NF-κB/nlrp3 signaling pathway and associated cytokine *** results from liver pathology,MRI assessments,and biochemical tests in rat models demonstrated YGJMF’s significant effectiveness in reducing liver damage and lipid ***,YGJMF markedly reduced hepatocyte inflammation by downregulating inflammatory cytokines in both liver tissue and ***,YGJMF was found to disrupt NF-κB activation,consequently inhibiting the assembly of the nlrp3 inflammasome in both the in vitro and in vivo *** preliminary findings of this study suggest that YGJMF may alleviate hepatic steatosis and inhibit the NF-κB/nlrp3 signaling pathway,thereby exerting anti-inflammatory effects in NASH.

关键词： Non-alcoholic steatohepatitis Nuclear factor kappa B nlrp3 inflammasome Yanggan Jiangmei Formula

nlrp3-mediated autophagy dysfunction links gut microbiota dysbiosis to tau pathology in chronic sleep deprivation

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Zoological Research 2024年第4期45卷 857-874页

作者： Na Zhao Xiu Chen Qiu-Gu Chen Xue-Ting Liu Fan Geng Meng-Meng Zhu Fu-Ling Yan Zhi-Jun Zhang Qing-Guo Ren Department of Neurology School of MedicineSoutheast UniversityNanjingJiangsu 210009China Department of Neurology Affiliated Zhongda HospitalSoutheast UniversityNanjingJiangsu 210009China

Emerging evidence indicates that sleep deprivation(SD)can lead to Alzheimer’s disease(AD)-related pathological changes and cognitive ***,the underlying mechanisms remain *** the present study,we identified the existence of a microbiota-gut-brain axis in cognitive deficits resulting from chronic SD and revealed a potential pathway by which gut microbiota affects cognitive functioning in chronic *** findings demonstrated that chronic SD in mice not only led to cognitive decline but also induced gut microbiota dysbiosis,elevated nlrp3 inflammasome expression,GSK-3βactivation,autophagy dysfunction,and tau hyperphosphorylation in the *** with the“SD microbiota”replicated the pathological and behavioral abnormalities observed in chronic sleep-deprived ***,both the deletion of nlrp3 in nlrp3-/-mice and specific knockdown of nlrp3 in the hippocampus restored autophagic flux,suppressed tau hyperphosphorylation,and ameliorated cognitive deficits induced by chronic SD,while GSK-3βactivity was not regulated by the nlrp3 inflammasome in chronic ***,deletion of nlrp3 reversed nlrp3 inflammasome activation,autophagy deficits,and tau hyperphosphorylation induced by GSK-3βactivation in primary hippocampal neurons,suggesting that GSK-3β,as a regulator of nlrp3-mediated autophagy dysfunction,plays a significant role in promoting tau ***,gut microbiota dysbiosis was identified as a contributor to chronic SD-induced tau pathology via nlrp3-mediated autophagy dysfunction,ultimately leading to cognitive ***,these findings highlight GSK-3βas a regulator of nlrp3-mediated autophagy dysfunction,playing a critical role in promoting tau hyperphosphorylation.

关键词： Chronic sleep deprivation Tau pathology nlrp3 inflammasome Autophagy GSK-3β Microbiota-gut-brain axis

nlrp3 and autophagy in retinal ganglion cell inflammation in age-related macular degeneration:potential therapeutic implications

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International Journal of Ophthalmology(English edition) 2024年第8期17卷 1531-1544页

作者： Xiao-Li Wang Yun-Xia Gao Qiong-Zhen Yuan Ming Zhang Department of Ophthalmology West China HospitalSichuan UniversityChengdu 610041Sichuan ProvinceChina

Retinal degenerative diseases were a large group of diseases characterized by the primary death of retinal ganglion cells(RGCs).Recent studies had shown an interaction between autophagy and nucleotide-binding oligomerization domain-like receptor 3(nlrp3)inflammasomes,which may affect RGCs in retinal degenerative *** nlrp3 inflammasome was a protein complex that,upon activation,produces caspase-1,mediating the apoptosis of retinal cells and promoting the occurrence and development of retinal degenerative *** autophagy could inhibit nlrp3 inflammasome activation,while inhibited autophagy can promote nlrp3 inflammasome activation,which leaded to the accelerated emergence of drusen and lipofuscin deposition under the neurosensory *** activated nlrp3 inflammasome could further inhibit autophagy,thus forming a vicious cycle that accelerated the damage and death of *** review discussed the relationship between nlrp3 inflammasome and autophagy and its effects on RGCs in age-related macular degeneration,providing a new perspective and direction for the treatment of retinal diseases.

关键词： autophagy age-related macular degeneration nlrp3 inflammasome retinal degeneration retinal ganglion cells

Telmisartan Reduced Cerebral Edema by Inhibiting nlrp_3 inflammasome in Mice with Cold Brain Injury

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2016年第4期36卷 576-583页

作者：魏欣胡晨晨张亚丽姚尚龙毛卫克 Department of Anesthesiology Union Hospital Tongji Medical College Huazhong University of Science and Technology

The aim of this study was to investigate the possible beneficial role of telmisartan in cerebral edema after traumatic brain injury（TBI） and the potential mechanisms related to the nucleotide-binding oligomerization domain（NOD）-like receptor（NLR） pyrin domain-containing 3（nlrp3） inflammasome activation. TBI model was established by cold-induced brain injury. Male C57BL/6 mice were randomly assigned into 3, 6, 12, 24, 48 and 72 h survival groups to investigate cerebral edema development with time and received 0, 5, 10, 20 and 40 mg/kg telmisartan by oral gavage, 1 h prior to TBI to determine the efficient anti-edemic dose. The therapeutic window was identified by post-treating 30 min, 1 h, 2 h and 4 h after TBI. Blood-brain barrier（BBB） integrity, the neurological function and histological injury were assessed, at the same time, the m RNA and protein expression levels of nlrp3 inflammasome, IL-1β and IL-18 concentrations in peri-contused brain tissue were measured 24 h post TBI. The results showed that the traumatic cerebral edema occurred from 6 h, reached the peak at 24 h and recovered to the baseline 72 h after TBI. A single oral dose of 5, 10 and 20 mg/kg telmisartan could reduce cerebral edema. Post-treatment up to 2 h effectively limited the edema development. Furthermore, prophylactic administration of telmisartan markedly inhibited BBB impairment, nlrp3, apoptotic speck-containing protein（ASC） and Caspase-1 activation, as well as IL-1β and IL-18 maturation, subsequently improved the neurological outcomes. In conclusion, telmisartan can reduce traumatic cerebral edema by inhibiting the nlrp3 inflammasome-regulated IL-1β and IL-18 accumulation.

关键词： telmisartan traumatic brain injury cerebral edema nlrp3 inflammasome inflammation

Heme oxygenase 1-mediated ferroptosis in Kupffer cells initiates liver injury during heat stroke

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ACTA PHARMACEUTICA SINICA B 2024年第9期14卷 3983-4000页

作者： Li, Ru Wei, Riqing Liu, Chenxin Zhang, Keying He, Sixiao Liu, Zhifeng Huang, Junhao Tang, Youyong An, Qiyuan Lin, Ligen Gan, Lishe Zhao, Liying Zou, Xiaoming Wang, Fudi Ping, Yuan Ma, Qiang Southern Med Univ Affiliated Hosp 7 Foshan 528244 Peoples R China Southern Med Univ Sch Lab Med & Biotechnol Dept Biopharmaceut Guangzhou 510000 Peoples R China Southern Med Univ Sch Lab Med & Biotechnol Guangdong Prov Key Lab Immune Regulat & Immunother Guangzhou 510000 Peoples R China Gen Hosp Southern Theatre Command PLA Med Crit Care Med Guangzhou 510000 Peoples R China Chinese Peoples Liberat Army Gen Hosp Natl Clin Res Ctr Geriatr Dis Guangdong Branch Ctr Guangzhou 510000 Peoples R China University Macao Inst Chinese Med Sci State Key Lab Qual Res Chinese Med Ave Univ Macau 999078 Peoples R China Zhejiang Chinese Med Univ Sch Pharmaceut Sci Hangzhou 311402 Peoples R China Southern Med Univ Nanfang Hosp Sch Clin Med 1 Dept Gen Surg Guangzhou 510000 Peoples R China Zhejiang Univ Affiliated Hosp 4 Affiliated Hosp 1 Inst Translat MedSch MedSch Publ HlthState Key Hangzhou 310000 Peoples R China Univ South China Affiliated Hosp 1 Affiliated Hosp 2 Hengyang Med SchSch Publ HlthBasic Med Sci Hengyang 421200 Peoples R China Zhejiang Univ Coll Pharmaceut Sci Hangzhou 310000 Peoples R China Zhejiang Univ Med Ctr Liangzhu Lab Hangzhou 310000 Peoples R China

With the escalating prevalence of global heat waves, heat stroke has become a prominent health concern, leading to substantial liver damage. Unlike other forms of liver injury, heat stroke-induced damage is characterized by heat cytotoxicity and heightened inflammation, directly contributing to elevated mortality rates. While clinical assessments have identified elevated bilirubin levels as indicative of Kupffer cell dysfunction, their specific correlation with heat stroke liver injury remains unclear. Our hypothesis proposes the involvement of Kupffer cell ferroptosis during heat stroke, initiating IL-1,beta-mediated inflammation. Using single-cell RNA sequencing of murine macrophages, a distinct and highly susceptible Kupffer cell subtype, Clec4F(+)/CD206(+), emerged, with heme oxygenase 1 (HMOX-1) playing a pivotal role. Mechanistically, heat-induced HMOX-1, regulated by early growth response factor 1, mediated ferroptosis in Kupffer cells, specifically in the Clec4F(+)/CD206(+) subtype (KC2), activating phosphatidylinositol 4-kinase beta and promoting PI4P production. This cascade triggered nlrp3 inflammasome activation and maturation of IL-1,beta. These findings underscore the critical role of targeted therapy against HMOX-1 in ferroptosis within Kupffer cells, particularly in Clec4F(+)/CD206(+) KCs. Such an approach has the potential to mitigate inflammation and alleviate acute liver injury in the context of heat stroke, offering a promising avenue for future therapeutic interventions. (c) 2024 The Authors. Published by Elsevier B.V. on behalf of Chinese Pharmaceutical Association andInstitute of Materia Medica, Chinese Academy of Medical Sciences.

关键词： Heat stroke Liver injury Kupffer cells Ferroptosis Heme oxygenase 1 Phosphatidylinositol 4-kinase beta nlrp3 Early growth response factor 1 nlrp3 inflammasome PROTECTIVE ROLE MACROPHAGES EXPRESSION HO-1 ACTIVATION IL-1-BETA DEATH SUSCEPTIBILITY PYROPTOSIS

Macrophage modulation with dipeptidyl peptidase-4 inhibitors:A new frontier for treating diabetic cardiomyopathy?

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World Journal of Diabetes 2024年第9期15卷 1847-1852页

作者： Saeed Mohammadi Ahmed Al-Harrasi Natural and Medical Sciences Research Center University of NizwaNizwa 616Oman Department of Biological Sciences and Chemistry University of NizwaNizwa 616Oman

This editorial introduces the potential of targeting macrophage function for diabetic cardiomyopathy(DCM)treatment by dipeptidyl peptidase-4(DPP-4)*** et al studied teneligliptin,a DPP-4 inhibitor used for diabetes management,and its potential cardioprotective effects in a diabetic mouse *** suggested teneligliptin administration may reverse established markers of DCM,including cardiac hypertrophy and compromised *** also inhibited the nlrp3 inflammasome and reduced inflammatory cytokine production in diabetic *** play crucial roles in DCM *** hyperglycemia disturbs the balance between pro-inflammatory(M1)and antiinflammatory(M2)macrophages,favoring a pro-inflammatory state contributing to heart ***,we highlight the potential of DPP-4 inhibitors to modulate macrophage function and promote an anti-inflammatory *** compounds may achieve this by elevating glucagon-like peptide-1 levels and potentially inhibiting the nlrp3 *** studies on teneligliptin in combination with other therapies targeting different aspects of DCM could be suggested for developing more effective treatment strategies to improve cardiovascular health in diabetic patients.

关键词： Diabetic cardiomyopathy Macrophage Dipeptidyl peptidase-4 inhibitor Teneligliptin nlrp3 inflammasome Glucagon-like peptide-1

Constituents from leaves of Macaranga hemsleyana

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Chinese Herbal Medicines 2024年第3期16卷 481-486页

作者： Joseph Sakah Kaunda Jia Liu Yaojun Xu Yuansi Chen Chenfang Yue Xingjie Zhang Ruihan Zhang Muhammad Amin Weilie Xiao Hongliang Li Xiaoli Li Key Laboratory of Medicinal Chemistry for Natural Resource Ministry of EducationYunnan Characteristic Plant Extraction LaboratoryYunnan Provincial Center for Research&Development of Natural ProductsState Key Laboratory for Conservation and Utilization of Bio-Resources in YunnanSchool of PharmacySchool of MedicineChemical Science and TechnologyYunnan UniversityKunming 650500China Yunnan Key Laboratory of Pharmacology for Natural Products Haiyuan CollegeKunming Medical UniversityKunming 650500China

Objective:To study constituents of the leaves of Macaranga hemsleyana,and evaluate their inhibitory effects against NOD-like receptor thermal protein domain associated protein 3(nlrp3)inflammasome activation,and antiproliferative ***:The constituents were isolated and purified by column chromatography on MCI gel CHP20P/P120,silica gel,Sephadex LH-20,and *** structures of compounds were determined by 1D,2D NMR,and HR-ESI-MS *** inhibitory effect of compounds on inflammasome activation was determined by lactate dehydrogenase(LDH)*** antiproliferative activity was evaluated using MTT ***:The study led to the isolation of 23 compounds,including one new compound,identified as(2Z)-3-[4-(β-D-glucopyranosyloxy)-2′-hydroxy-5′-methoxyphenyl]-2-propenoic acid(1),together with 22 known compounds recognized as 1,4-dihydro-4-oxo-3-pyridinecarbonitrile(2),methyl 4-methoxynicotinate(3),4-methoxynicotinonitrile(4),1-(3-O-β-D-glucopyranosyl-4,5-dihydroxyphenyl)-ethanone(5),neoisoastilbin(6),isoastilbin(7),aromadendrin(8),neoastilbin(9),astilbin(10),quercitrin(11),neoschaftoside(12),apigenin 6,8-bis-C-α-L-arabinoside(13),vitexin(14),bergenin(15),scopoletin(16),glucopyranoside salicyl(17),koaburside(18),benzylβ-D-glucoside(19),icariside B5(20),roseoside(21),loliolide(22),and adenosine(23).The tested compounds did not show LDH inhibition nor antiproliferative ***:Compound 1 was a new *** 2 and 3 were obtained for the first time from natural *** 22 known compounds constituted of alkaloids(2–4,23),phenolics(5,15,17,18),flavonoids(6–14),coumarin(16),benzyl glycoside(19),and norsesquiterpenes(20–22).All the compounds,1–23,were revealed from *** for the first *** is the initial uncovering of molecules 1–10,12,13,17–19,and 23 from the genus *** isolated compounds,11,14–16,and 20–22 established taxonomic classification of *** in Euphorbiaceae *** were outstanding as

关键词： antiproliferative activity chemotaxonomic significance flavonoids glycoside Macaranga hemsleyana Pax et Hoffm nlrp3 inflammasome

TAX1BP1 protects against myocardial infarction-associated cardiac anomalies through inhibition of inflammasomes in a RNF34/MAVS/nlrp3-dependent manner

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Science Bulletin 2021年第16期66卷 1669-1683,M0004页

作者： Haixia Xu Wenjun Yu Shiqun Sun Congye Li Jun Ren Yingmei Zhang Department of Cardiology Zhongshan HospitalFudan UniversityShanghai Institute of Cardiovascular DiseasesShanghai 200032China Department of Cardiology Affiliated Hospital of Nantong UniversityNantong 226001China Department of Cardiology Xijing HospitalAir Force Military Medical UniversityXi’an 710038China Department of Pathology University of WashingtonSeattle WA 98195USA

Acute myocardial infarction(MI),one of the most common cardiovascular emergencies,is a leading cause of morbidity and *** evidence has revealed an essential role for inflammasome activation and autophagy in the pathogenesis of acute ***1-binding protein 1(TAX1BP1),an adaptor molecule involved in termination of proinflammatory signaling,serves as an important selective autophagy adaptor,but its role in cardiac ischemia remains *** study examined the role of TAX1BP1 in myocardial ischemic stress and the underlying mechanisms *** of TAX1BP1 were significantly downregulated in heart tissues of patients with ischemic heart disease and in a left anterior descending(LAD)ligation-induced model of acute *** carrying TAX1BP1 was delivered into the *** acute MI induced procedure elicited an infarct and cardiac dysfunction,the effect of which was mitigated by TAX1BP1 overexpression with little effect from viral vector ***1BP1 nullified acute MI-induced activation of the nlrp3 inflammasome and associated mitochondrial ***1BP1 overexpression suppressed nlrp3 mitochondrial localization by inhibiting the interaction of nlrp3 with mitochondrial antiviral signaling protein(MAVS).Further investigation revealed that ring finger protein 34(RNF34)was recruited to interact with TAX1BP1 thereby facilitating autophagic degradation of MAVS through K27-linked polyubiquitination of *** of RNF34 using siRNA nullified TAX1BP1 yielded protection against hypoxia-induced MAVS mitochondrial accumulation,nlrp3 inflammasome activation and associated loss of mitochondrial membrane *** together,our results favor a cardioprotective role for TAX1BP1 in acute MI through repression of inflammasome activation in a RNF34/MAVS-dependent manner.

关键词： TAX1BP1 Acute myocardial infarction nlrp3 inflammasome Mitochondrial antiviral signaling protein RNF34 Autophagic degradation