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Activation of NLRP3 Inflammasome via Drp1 Overexpression in kupffer cells Aggravates Ischemia-reperfusion Injury in Hepatic Steatosis

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Journal of Clinical and Translational Hepatology 2023年第5期11卷 1069-1078页

作者： Lu Zhang Mingfu Wang Ran An Jun Dai Shujun Liu Ming Chen Haoran Ding Department of Hepatobiliary Surgery Affiliated Drum Tower Hospital of Nanjing University Medical SchoolNanjingJiangsuChina Surgery Department I Zhangjiagang Traditional Chinese Medicine HospitalSuzhouJiangsuChina Department of Hepatobiliary Surgery The First Affiliated Hospital of Wannan Medical CollegeWuhuAnhuiChina Department of Hepatobiliary Surgery Nanjing Drum Tower HospitalClinical College of Traditional Chinese and Western MedicineSchool of PharmacyNanjing University of Chinese MedicineNanjingJiangsuChina

Background and Aims:Donors with fatty livers are considered to address the shortage of livers for transplantation,but those livers are particularly sensitive to ischemia-reperfusion injury(IRI),and an increased incidence of graft failure is *** cells account for 20–35%of liver nonparenchymal cells,and have been shown to participate in the process of IRI and inflammatory reactions of hepatic ***-like receptor thermal protein domain-associated protein 3(NLRP3)is an intracellular sensor activated by kupffer cells to promote generation and participates in ***-associated protein 1(Drp1)is one of the main proteins regulating mitochondrial division and exacerbates IRI by affecting mitochondrial *** mechanism of interaction of kupffer cells with Drp1 and NLRP3 to aggravate IRI has not been ***:A mouse model of hepatic steatosis was established by feeding the mice with a high-fat *** vitro experiments were performed using AML12 normal mouse liver cells and RAW264.7 mononuclear macrophage cells cultured in medium with palmitate and oleic *** blotting and immunohistochemical(IHC)staining were used to detect the expression of NLRPP3 and Drp1 in IRI in the control and high-fat diet *** expression of F4/80+cells during IRI in hepatic steatosis was verified by IHC staining,and the role of NLRPP3 and Drp1 in kupffer-cell mediated IRI was investigated by targeting Drp-1 ***:Drp1 and NLRP3 expression was increased during IRI in hepatic steatosis,and the expression of Drp1 and NLRP3 were decreased after the elimination of kupffer *** indicated kupffer cells were involved in the process of IRI in hepatic steatosis through the action of Drp1 and *** Drp1 inhibition,liver function was restored and NLRP3 expression level was ***:kupffer cells aggravated IRI in hepatic steatosis via NLRP3 and ***1 inhibitors might be useful as specific therapeutics to alleviate IRI

关键词： Drp1 kupffer cells NLRP3 Hepatic steatosis Ischemia-reperfusion

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Effects of Different Therapeutic Methods and Typical Recipes of Chinese Medicine on Activation of c-Jun N-terminal Kinase in kupffer cells of Rats with Fatty Liver Disease

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Chinese Journal of Integrative Medicine 2012年第10期18卷 769-774页

作者：杨钦河胡四平张玉佩平换换杨环文陈同炎刘海涛 Department of Traditional Chinese Medicine Medical CollegeJinan University Qingyuan Maternity and Child Health Care Hospital

Objective： To observe the effects of different therapeutic methods and the recipes of Chinese medicine （CM） on the activation of c-Jun N-terminal kinase （JNK） in kupffer cells of rats with fatty liver disease and to explore the mechanisms of these therapeutic methods. Methods： By using a random number table, 98 rats were randomly divided into 7 groups： control group, model group, and 5 treatment groups, including soothing Liver （Gan） recipe group, invigorating Spleen （Pi） recipe group, dispelling dampness recipe group, promoting blood recipe group, and complex recipe group. Rats in the control group were fed with normal food and distilled water by gastric perfusion, while rats in the model group were fed with high-fat food and distilled spirits by gastric perfusion. Rats in the 5 treatment groups were fed with high-fat food and corresponding recipes by gastric perfusion. Twelve weeks later, all rats were sacrificed and liver tissues were stained for pathohistological observation. kupffer cells were isolated from livers of rats to evaluate JNK and phospho-JNK expressions by Western blotting. Results： The grade of hepatic steatosis was higher in the model group than the control group （P〈0.05）. Compared with the model group, the grade of fatty degeneration in soothing Liver recipe group and invigorating Spleen recipe group were significantly ameliorated （P〈0.05）. Expressions of JNK and phospho-JNK in kupffer cells were significantly higher in the model group than those in the control group （P〈0.05, P〈0.01）. Compared with the model group, expressions of JNK in all treatment groups decreased, especially in invigorating Spleen recipe group and promoting blood recipe group （P〈0.05）. Compared with the model group, expressions of phospho-JNK in all treatment groups declined significantly （P〈0.01）, especially in soothing Live recipe group and invigorating Spleen recipe group. Conclusions： The high expressions of JNK and phospho-JNK in kupffer cells might play an important rol

关键词： fatty liver disease Chinese medicine kupffer cells c-Jun N-terminal kinase

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Role of kupffer cells in the pathogenesis of liver disease

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World Journal of Gastroenterology 2006年第46期12卷 7413-7420页

作者： George Kolios Vassilis Valatas Elias Kouroumalis Depart-ment of Gastroenterology and Hepatology University Hospital and Medical School University of Crete Heraklion Greece

kupffer cells, the resident liver macrophages have long been considered as mostly scavenger cells responsible for removing particulate material from the portal circulation. However, evidence derived mostly from animal models, indicates that kupffer cells may be implicated in the pathogenesis of various liver diseases including viral hepatitis, steatohepatitis, alcoholic liver disease, intrahepatic cholostasis, activation or rejection of the liver during liver transplantation and liver fibrosis. There is accumulating evidence, reviewed in this paper, suggesting that kupffer cells may act both as effector cells in the destruction of hepatocytes by produdng harmful soluble mediators as well as antigen presenting cells during viral infections of the liver. Moreover they may represent a significant source of chemoattractant molecules for cytotoxic CD8 and regulatory T cells. Their role in fibrosis is well established as they are one of the main sources of TGFβ1 production, which leads to the transformation of stellate cells into myofibroblasts. Whether all these variable functions in the liver are mediated by different kupffer cell subpopulations remains to be evaluated. In this review we propose a model that demonstrates the role of kupffer cells in the pathogenesis of liver disease.

关键词： kupffer cells Liver disease Hepatic injury Liver fibrosis Hepatocellular carcinoma Hepatitis Steatohepatitis

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Ron receptor-dependent gene regulation of kupffer cells during endotoxemia

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Hepatobiliary & Pancreatic Diseases International 2014年第3期13卷 281-292页

作者： Rishikesh M Kulkarni William D Stuart Susan E Waltz Department of Cancer Biology University of Cincinnati Department of Research Cincinnati Veterans Affairs Medical Center

BACKGROUND: Ron receptor tyrosine kinase signaling in macrophages, including kupffer cells and alveolar macrophages,suppresses endotoxin-induced proinflammatory cytokine/chemokine production. Further, we have also identified genes from Ron replete and Ron deplete livers that were differentially expressed during the progression of liver inflammation associated with acute liver failure in mice by microarray *** important genes and signaling pathways have been identified downstream of Ron signaling during progression of inflammation by this approach, the precise role that Ron receptor plays in regulating the transcriptional landscape in macrophages, and particular in isolated kupffer cells, has still not been ***: kupffer cells were isolated from wild-type(TK+/+)and Ron tyrosine kinase deficient(TK-/-) mice. Ex vivo, the cells were treated with lipopolysaccharide(LPS) in the presence or absence of the Ron ligand, hepatocyte growth factor-like protein(HGFL). Microarray and qRT-PCR analyses were utilized to identify alterations in gene expression between ***: Microarray analyses identified genes expressed differentially in TK+/+ and TK-/- kupffer cells basally as well as after HGFL and LPS treatment. Interestingly, our studies identified Mefv, a gene that codes for the anti-inflammatory protein pyrin, as an HGFL-stimulated Ron-dependent ***, lipocalin 2, a proinflammatory gene, which is induced by LPS, was significantly suppressed by HGFL *** results were validated by qRT-PCR studies on kupffer cells treated with LPS and ***: The studies herein suggest a novel mechanism whereby HGFL-induced Ron receptor activation promotes the expression of anti-inflammatory genes while inhibiting genes involved in inflammation with a net effect of diminished inflammation in macrophages.

关键词： Mst1R Mefv Lcn2 Met receptor kupffer cells macrophages

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Donor denervation and elimination of kupffer cells affect expression of P-selectin and ICAM-1 in liver graft

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Hepatobiliary & Pancreatic Diseases International 2007年第4期6卷 379-382页

作者： Zhu, Hong Guo, Yong-Zhang Zhang, Jie Hu, Ming-Dao Tang, Ji-Hong Tian, Da-Guang Yong-Jun, A. Sun, Feng Wei, Xiao-Ping Kunming Med Coll Affiliated Hosp 2 Div Hepatobiliary Dept 1 Kunming 650101 Peoples R China

BACKGROUND: The non-function and dysfunction of primary liver graft likely involves dependence on kupffer cells and hepatic innervation. The present experiment was designed to study the expression of P-selectin and intercellular adhesion molecule-1 (ICAM-1) mRNA in liver graft and to elucidate the role of kupffer cells and the sympathetic nerve of the liver in down-regulating this expression. METHODS: Donor rats were given hexamethonium, a sympathetic ganglionic blocking agent, and/or gadolinium chloride, an inhibitor of kupffer cells. Then the changes of graft P-selectin and ICAM-1 mRNA expression were measured after liver transplantation. RESULTS: The expressions of P-selectin and ICAM-1 mRNA were increased after liver transplantation, and down-regulated by liver denervation and elimination of kupffer cells. CONCLUSIONS: Live donor denervation and elimination of kupffer cells down-regulated the expressions of P-selectin and ICAM-1 mRNA in grafts. This may decrease graft ischemia/reperfusion injury.

关键词： liver transplantation hepatic nerve kupffer cells reperfusion injury adhesion molecule

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The regulatory effect of ERK1/2 signal pathway on production of TNFα induced by LPS in mice kupffer cells

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Chinese Journal of Traumatology 2001年第3期4卷 139-142页

作者：张宇蒋建新吉善和单佑安朱佩芳周继红 Research Institute of Surgery Daping Hospital Third Military Medical University Chongqing 400042 China.

Objective: To study the rule of ERK1/2 activity and regulative effect of ERK1/2 pathway on the production of pro inflammatory cytokine TNFα in mice kupffer cells (mKC) induced by LPS, and to exploring novel methods to prevent and treat clinical patients of endotoxemia. Methods: Immunoprecipitate kinase assay and Western blotting analysis were used to detect the phosphorylated ERK1/2 kinase activity in mKC stimulated by LPS, and ELISA was used to study the effect of ERK1/2 signaling cascade on LPS induced TNFα production in mKC. Results: In mKC, LPS treatment resulted in transient and rapid increase of kinase activity of ERK1/2 that phosphorylated their specific substrate ELK 1, with maximal value at 30 minutes and a return near to baseline within 2 hours, and LPS induced ERK1/2 activity from LPS concentration of 10 pg/ml to the top activity at 100 ng/ml . No activity was observed in unstimulated mKC. Inhibition of the ERK1/2 pathway using the specific ERK 1/2 signal pathway inhibitor PD98059 caused a marked and concentration dependent reduction of TNFα production. Conclusions: The results show that LPS can markedly activate ERK1/2 pathway in mKC. PD98059 causes a significant and concentration dependent reduction of TNFα production. ERK1/2 may be a novel target to treat clinical patient of endotoxemia.

关键词： kupffer cells Lipopolysaccharides Tumor necrosis factor Extracellular signal regulated kinase

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The polarizable and reprogrammable identity of kupffer cells in Nonalcoholic Steatohepatitis

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Medical Review 2022年第4期2卷 324-327页

作者： Tarik Zahr Kevin Sun Li Qiang Naomi Berrie Diabetes Center Columbia University1150 St.Nicholas AveNew YorkNY 10032USA Department of Molecular Pharmacology and Therapeutics Columbia UniversityNew YorkNYUSA Department of Pathology and Cell Biology Columbia UniversityNew YorkNY 10032USA

kupffer cells(KCs)are the resident macrophages of the liver with similar origins to myeloid-derived *** differentiated,KCs exhibit distinct cellular machinery capable of longevity and self-renewal,making them a crucial player in promoting effective intrahepatic ***,this gets compromised in disease states like Nonalcoholic Steatohepatitis(NASH),where the loss of embryo-derived KCs(EmKCs)is *** this,other KC-like and KC-derived populations start to form and contribute to a variety of roles in NASH pathogenesis,often adopting a NASH-associated molecular *** we offer a brief overview of recent reports describing KC polarization and reprogramming in the *** describe the complexities of KC cellular identity,their proposed ability to reprogram to fibroblast-like and endothelial-like cells,and the potential implications in NASH.

关键词： kupffer cells macrophages Nonalcoholic Steatohepatitis polarization reprogramming

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Early use of dexamethasone increases Nr4a1 in kupffer cells ameliorating acute liver failure in mice in a glucocorticoid receptor-dependent manner

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Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2020年第9期21卷 727-739页

作者： Jing-wen DENG Qin YANG Xiao-peng CAI Jia-ming ZHOU Wei-gao E Yan-dong AN Qiu-xian ZHENG Meng HONG Yan-li REN Jun GUAN Gang WANG Shu-jing LAI Zhi CHEN State Key Laboratory for Diagnosis and Treatment of Infectious Diseases National Clinical Research Center for Infectious DiseasesCollaborative Innovation Center for Diagnosis and Treatment of Infectious Diseasesthe First Affiliated HospitalSchool of MedicineZhejiang UniversityHangzhou 310003China Center for Stem Cell and Regenerative Medicine Zhejiang University School of MedicineHangzhou 310058China Becton Dickinson and CompanyShanghai 200126China

Background and objective:Acute liver failure(ALF)is a type of disease with high mortality and rapid progression with no specific treatment methods currently *** exert beneficial clinical effects on therapy for ***,the mechanism of this effect remains unclear and when to use glucocorticoids in patients with ALF is difficult to *** purpose of this study was to investigate the specific immunological mechanism of dexamethasone(Dex)on treatment of ALF induced by lipopolysaccharide(LPS)/D-galactosamine(D-Ga IN)in ***:Male C57 BL/6 mice were given LPS and D-Ga IN by intraperitoneal injection to establish an animal model of *** was administrated to these mice and its therapeutic effect was *** and eosin(H&E)staining was used to determine liver *** flow cytometry,cytometric bead array(CBA)method,and next-generation sequencing were performed to detect changes of messenger RNA(m RNA)in immune cells,cytokines,and kupffer cells,***:A mouse model of ALF can be constructed successfully using LPS/D-Ga IN,which causes a cytokine storm in early disease *** immune cells change markedly with progression of liver *** use of Dex,at 0 h rather than 1 h,could significantly improve the progression of ALF induced by LPS/D-Ga IN in *** of innate immune cells,especially kupffer cells and neutrophils,increased significantly in the Dex-treated *** vivo experiments indicated that the therapeutic effect of Dex is exerted mainly via the glucocorticoid receptor(Gr).Sequencing of kupffer cells revealed that Dex could increase m RNA transcription level of nuclear receptor subfamily 4 group A member 1(Nr4 a1),and that this effect disappeared after Gr ***:In LPS/D-Ga IN-induced ALF mice,early administration of Dex improved ALF by increasing the numbers of innate immune cells,especially kupffer cells and ***-dependent Nr4 a1 upregul

关键词： Glucocorticoid Dexamethasone kupffer cells Acute liver failure Nuclear receptor subfamily 4 group A member 1(Nr4a1)

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kupffer cells promote the differentiation of adult liver hematopoietic stem and progenitor cells into lymphocytes via ICAM-1 and LFA-1 interaction

Kupffer cells promote the differentiation of adult liver hem...

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第十三届全国免疫学学术大会

作者： Deping Meng Yuhong Qin Nan Lu Keke Fang Zhigang Tian Cai Zhang Institute of Immunopharmacology and Immunotherapy School of Pharmaceutical SciencesShandong University Institute of Diagnostics School of MedicineShandong University Institute of Immunology School of Life SciencesUniversity of Science and Technology of China

It has been reported that the adult liver contains hematopoietic stem and progenitor cells(HSPCs), which are associated with long-term hematopoietic reconstitution activity. Hepatic hematopoiesis plays an important role in the generation of cells involved in tumor surveillance and rejection. However, how the progenitors differentiate into functional myeloid cells and lymphocytes in the liver microenvironment remains unknown. In the present study, HSPC transplantation experiments were used to confirm that adult murine liver HSPCs differentiate into both myeloid cells and lymphocytes(preferentially T cells) compared with bone marrow HSPCs. Using a coculture system comprised of kupffer cells and HSPCs, we found that kupffer cells promote adult liver HSPCs to primarily generate T cells and B cells. We then demonstrated that kupffer cells can also promote HSPC expansion. A blockade of intercellular cell adhesion molecule-1(ICAM-1) in a liver HSPC and kupffer cell coculture system impaired the adhesion, expansion, and differentiation of HSPCs. These results suggest a critical role of kupffer cells in the maintenance and promotion of adult mouse liver hematopoiesis. These findings provide important insight into understanding liver extramedullary hematopoiesis and its significance, particularly regarding therapy for liver tumors and immune rejection during organ transplantation.

关键词： Liver HSPC kupffer cells ICAM-1 LSK

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Role of liver X receptors alpha agonist on expressions of LPS-induced inflammatory response associated factor IRAK-4 and NF-kappaB in kupffer cells

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Journal of Medical Colleges of PLA(China) 2008年第2期23卷 70-75页

作者： Wang Ding Miao Chunmu Gong Jianping Department of Hepatobiliary Surgery Second Affiliated Hospital of Chongqing Medical University Chongqing 400010 China

Objective： To explore the role of activated liver X receptor α （LXRα） on the expressions of interleukin-1 receptor associated kinase-4 （IRAK-4） and NF-kappaB （NF-κB） in the inflammatory response which induced by LPS in the kupffer cells and to investigate the possible mechanisms of LXRα negative regulation of inflammatory response. Methods： The kupffer cells were isolated from male Kunming mice by collagen perfusion in situ. And these cells were divided into 4 groups： normal control group, LPS treatment group, LXRct agonist T0901317 treatment group, LPS and T0901317 combined treatment group. The LPS treatment group were treated with a final concentration of 1 μg/ml LPS in RPMI 1640 and cultured for 6 h, the T0901317 treatment group were treated with a final concentration of 5 μg/ml in RPMI 1640 and cultured for 24 h, and the combined treatment group received pre-culture for 24 h with a final concentration of 1μg/ml T0901317 in RPMI 1640 and then cultured for 6 h with a final concentration of 5 μg/ml LPS in RPMI 1640. All groups were cultured for 30 h. The expression of LXRα, IRAK-4 and NF-κB at mRNA and protein levels were detected by real-time PCR and Western blotting, and the TNF-α and IL-1β levels were detected by ELISA. Results： The levels of LXRα mRNA and protein were highest in T0901317 group, and lowest in LPS group （P〈0.05）. The level of IRAK4 and NF-κB mRNAs and proteins were evidently lower in the Combined-treated group than in LPS group （P〈0.05）. And the level of TNF-α and IL-1 were observed highest in LPS group （P〈0.05）, but no difference among the Control group, T0901317 group and Combined-treated group （P〉0.05）. Conclusion： These date suggest that the LXR agonists can effectively up-regulate the expressions of LXRα mRNA and protein and inhibit the inflammatory response. This may be via down-regulating the expressions of IRAK4 and NF-κB at mRNA and protein levels.

关键词： Liver X receptors kupffer cells Inflammation Interleukin-1 receptor associated kinase-4 NF-kappaB

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