Gao-Binge模型在酒精性肝病研究领域应用现状及未来前景

周珂; 王华

doi:10.3969/j.issn.1001-5256.2019.03.007

Gao-Binge模型在酒精性肝病研究领域应用现状及未来前景

DOI: 10.3969/j.issn.1001-5256.2019.03.007

周珂,
王华

1. 安徽医科大学药学院肝病研究所
2. 安徽医科大学第一附属医院肿瘤科

基金项目:

国家自然科学基金优秀青年基金(81522009/H0317);国家自然科学基金上项目(81770588/H0315)；

详细信息

中图分类号: R575
计量
- 文章访问数: 2410
- HTML全文浏览量: 115
- PDF下载量: 513
- 被引次数: 0
出版历程
- 出版日期: 2019-03-20

Application status and future prospect of the Gao-Binge model in alcoholic liver disease

Zhou Ke,
Wang Hua

School of Pharmacy, Institute of Liver Diseases, Anhui Medical University

Research funding:

摘要

摘要:
酒精性肝病的发病机制一直不明确,主要原因之一是现有的研究中始终缺乏精准合适的动物模型来模拟整个疾病病程。在探究酒精性肝病发病机制以及可能的治疗措施过程中,已经构建过多种不同的动物模型来模拟酒精性肝病,但都存在利弊。其中Gao-Binge模型因为更接近人类饮酒模式而受到业界广泛认可及应用,通过该模型研究发病机制和探寻潜在治疗药物更具说服力。Gao-Binge模型具有造模周期短、成本低、重复性好的优势,尽管存在一些局限性,如无法模拟酒精性肝病更严重的疾病进程,但是该模型在酒精性肝病研究中的价值毋庸置疑,而且在研究酒精导致其他器官损伤（包括心脏、胰腺）以及脂肪组织损伤中亦前景广阔。
- 肝疾病,酒精性 /
- 模型,动物 /
- Gao-Binge模型
Abstract:
The pathogenesis of alcoholic liver disease remains unclear, mainly due to the lack of accurate animal models in experiments.Many different animal models have been established to mimic alcoholic liver disease in patients, which have both advantages and disadvanta-ges. Among these models, the Gao-Binge model is widely used in the experiments because it highly mimics the drinking pattern in patients.It is more persuasive that the pathogenesis and therapeutic drugs have been examined in the Gao-Bingemodel. Although there are some lim-its in the Gao-Binge model, it is no doubt that this model has high value and future prospect in the study of alcoholic liver disease becauseof short duration time, low cost and good repeatability. Finally, the Gao-Binge model has also been used to study alcohol-induced damageto other organs such as the heart, pancreas, adipose tissue etc.
- liver diseases, alcoholic /
- models, animal /
- Gao-Binge model

HTML全文

参考文献(33)

[1] OSNA NA, DONOHUE TM Jr, KHARBANDA KK. Kharbanda, alcoholic liver disease:Pathogenesis and current management[J]. Alcohol Res, 2017, 38 (2) :147-161.

[2] GAO B, BATALLER R. Alcoholic liver disease:Pathogenesisand new therapeutic targets[J]. Gastroenterology, 2011, 141 (5) :1572-1585.

[3] BUKONG TN, CHO Y, IRACHETA-VELLVE A, et al. Abnor-mal neutrophil traps and impaired efferocytosis contribute toliver injury and sepsis severity after binge alcohol use[J]. JHepatol, 2018, 69 (5) :1145-1154.

[4] ZHOU H, YU M, ZHAO J, et al. IRAKM-Mincle axis links celldeath to inflammation:Pathophysiological implications forchronic alcoholic liver disease[J]. Hepatology, 2016, 64 (6) :1978-1993.

[5] UENO A, LAZARO R, WANG PY, et al. Mouse intragastric in-fusion (i G) model[J]. Nat Protoc, 2012, 7 (4) :771-781.

[6] BERTOLA A, MATHEWS S, KI SH, et al. Mouse model ofchronic and binge ethanol feeding (the NIAAA model) [J].Nat Protoc, 2013, 8 (3) :627-637.

[7] XU MJ, CAI Y, WANG H, et al. Fat-specific protein 27/CI-DEC promotes development of alcoholic steatohepatitis in miceand humans[J]. Gastroenterology, 2015, 149 (4) :1030-1041. e6.

[8] DONEPUDI AC, FERRELL JM, BOEHME S, et al. Deficiencyof cholesterol 7alpha-hydroxylase in bile acid synthesis exac-erbates alcohol-induced liver injury in mice[J]. HepatolCommun, 2018, 2 (1) :99-112.

[9] CHEN H, SHEN F, SHERBAN A, et al. DEP domain-contai-ning m TOR-interacting protein suppresses lipogenesis and a-meliorates hepatic steatosis and acute-on-chronic liver inju-ry in alcoholic liver disease[J]. Hepatology, 2018, 68 (2) :496-514.

[10] ZHANG D, TONG X, NELSON BB, et al. The hepatic BMAL1/AKT/lipogenesis axis protects against alcoholic liver disease inmice via promoting PPARalpha pathway[J]. Hepatology, 2018.[Epub ahead of print][11] SATISHCHANDRAN A, AMBADE A, RAO S, et al. MicroRNA122, regulated by GRLH2, protects livers of mice and patientsfrom ethanol-induced liver disease[J]. Gastroenterology, 2018, 154 (1) :238-252. e7.

[12] BERTOLA A, PARK O, GAO B. Chronic plus binge ethanolfeeding synergistically induces neutrophil infiltration and liverinjury in mice:A critical role for E-selectin[J]. Hepatology, 2013, 58 (5) :1814-1823.

[13] ROH YS, ZHANG B, LOOMBA R, et al. TLR2 and TLR9 con-tribute to alcohol-mediated liver injury through induction ofCXCL1 and neutrophil infiltration[J]. Am J Physiol GastrointestLiver Physiol, 2015, 309 (1) :g30-g41.

[14] LI M, HE Y, ZHOU Z, et al. MicroRNA-223 ameliorates alco-holic liver injury by inhibiting the IL-6-p47 (phox) -oxidativestress pathway in neutrophils[J]. Gut, 2017, 66 (4) :705-715.

[15] LOUVET A, MATHURIN P. Mathurin, alcoholic liver disease:Mechanisms of injury and targeted treatment[J]. Nat RevGastroenterol Hepatol, 2015, 12 (4) :231-242.

[16] WANG M, SHEN G, XU L, et al. IL-1 receptor like 1 protectsagainst alcoholic liver injury by limiting NF-κB activation in he-patic macrophages[J]. J Hepatol, 2018, 68 (1) :109-117.

[17] KHANOVA E, WU R, WANG W, et al. Pyroptosis by caspase11/4-gasdermin-D pathway in alcoholic hepatitis in mice and pa-tients[J]. Hepatology, 2018, 67 (5) :1737-1753.

[18] CHEN Y, OUYANG X, HOQUE R, et al.β-Hydroxybutyrateprotects from alcohol-induced liver injury via a Hcar2-cAMPdependent pathway[J]. J Hepatol, 2018, 69 (3) :687-696.

[19] HARTMANN P, HOCHRATH K, HORVATH A, et al. Modulationof the intestinal bile acid/farnesoid X receptor/fibroblastgrowth factor 15 axis improves alcoholic liver disease in mice[J]. Hepatology, 2018, 67 (6) :2150-2166.

[20] GRANDER C, ADOLPH TE, WIESER V, et al. Recovery ofethanol-induced Akkermansia muciniphila depletion amelio-rates alcoholic liver disease[J]. Gut, 2018, 67 (5) :891-901.

[21] BUKONG TN, IRACHETA-VELLVE A, SAHA B, et al. Inhibi-tion of spleen tyrosine kinase activation ameliorates inflamma-tion, cell death, and steatosis in alcoholic liver disease[J].Hepatology, 2016, 64 (4) :1057-1071.

[22] KI SH, PARK O, ZHENG M, et al. Interleukin-22 treatment a-meliorates alcoholic liver injury in a murine model of chronic-binge ethanol feeding:Role of signal transducer and activatorof transcription 3[J]. Hepatology, 2010, 52 (4) :1291-1300.

[23] BLAYA D, COLL M, RODRIGO-TORRES D, et al. IntegrativemicroRNA profiling in alcoholic hepatitis reveals a role for mi-croRNA-182 in liver injury and inflammation[J]. Gut, 2016, 65 (9) :1535-1545.

[24] LLORENTE C, JEPSEN P, INAMINE T, et al. Gastric acidsuppression promotes alcoholic liver disease by inducing o-vergrowth of intestinal Enterococcus[J]. Nat Commun, 2017, 8 (1) :837.

[25] CAI Y, XU MJ, KORITZINSKY EH, et al. Mitochondrial DNA-enriched microparticles promote acute-on-chronic alcoholicneutrophilia and hepatotoxicity[J]. JCI Insight, 2017, 2 (14) .[Epub ahead of print][26] EGUCHI A, LAZARO RG, WANG J, et al. Extracellular vesi-cles released by hepatocytes from gastric infusion model of al-coholic liver disease contain a MicroRNA barcode that can bedetected in blood[J]. Hepatology, 2017, 65 (2) :475-490.

[27] SUN Q, ZHANG W, ZHONG W, et al. Pharmacological inhibi-tion of NOX4 ameliorates alcohol-induced liver injury in micethrough improving oxidative stress and mitochondrial function[J]. Biochim Biophys Acta, 2017, 1861 (1 Pt A) :2912-2921.

[28] MUKHOPADHYAY P, HORVTH B, RAJESH M, et al. PARPinhibition protects against alcoholic and non-alcoholic steato-hepatitis[J]. J Hepatol, 2017, 66 (3) :589-600.

[29] ZHOU C, LAI Y, HUANG P, et al. Naringin attenuates alco-holic liver injury by reducing lipid accumulation and oxidativestress[J]. Life Sci, 2019, 216:305-312.

[30] ADEJUMO AC, AJAYI TO, ADEGBALA OM, et al. Cannabisuse is associated with reduced prevalence of progressive sta-ges of alcoholic liver disease[J]. Liver Int, 2018, 38 (8) :1475-1486.

[31] VARGA ZV, MATYAS C, PALOCZI J, et al. Alcohol misuseand kidney injury:Epidemiological evidence and potentialmechanisms[J]. Alcohol Res, 2017, 38 (2) :283-288.

[32] MATYAS C, VARGA ZV, MUKHOPADHYAY P, et al. Chronicplus binge ethanol feeding induces myocardial oxidativestress, mitochondrial and cardiovascular dysfunction, andsteatosis[J]. Am J Physiol Heart Circ Physiol, 2016, 310 (11) :h1658-h1670.

[33] LI Y, WANG S, NI HM, et al. Autophagy in alcohol-inducedmultiorgan injury:Mechanisms and potential therapeutic tar-gets[J]. Biomed Res Int, 2014, 2014:498491.

[34] MATHEWS S, XU M, WANG H, et al. Animals models of gas-trointestinal and liver diseases. Animal models of alcohol-in-duced liver disease:pathophysiology, translational relevance, and challenges[J]. Am J Physiol Gastrointest Liver Physiol, 2014, 306 (10) :g819-g823.

[35] GAO B, XU MJ, BERTOLA A. et al. Animal models of alcohol-ic liver disease:Pathogenesis and clinical relevanc[J]. GeneExpr, 2017, 17 (3) :173-186.

施引文献

资源附件(0)

访问统计