肝血窦在内毒素致肝损伤中的作用

赵利利; 袁东亚; 孙芳云

doi:10.3969/j.issn.1001-5256.2016.01.040

肝血窦在内毒素致肝损伤中的作用

DOI: 10.3969/j.issn.1001-5256.2016.01.040

西藏民族大学医学院生命科学基础研究实验室

基金项目:

2014年西藏自治区科技厅自然科学基金项目；

详细信息

中图分类号: R575
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- 文章访问数: 1943
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- 被引次数: 0
出版历程
- 收稿日期: 2015-06-04
- 出版日期: 2016-01-20

Role of hepatic sinusoids in lipopolysaccharide-induced liver injury

Lab for Basic Research of Life Science,Xizang Minzu University

Research funding:

摘要

摘要: 内毒素是革兰阴性菌细胞壁中的特有成分,又称脂多糖(LPS)。肝脏既是清除细菌和内毒素的场所,又是最易受损的器官。肝损伤最初发生在肝血窦。主要介绍了LPS对Kupffer细胞、肝窦内皮细胞、肝血窦中氧化/抗氧化平衡及肝脏血流的影响。认为肝血窦在LPS所造成的肝损伤中的作用不容忽视,研究其对防治LPS致肝损伤有重要意义。
- 肝疾病 /
- 脂多糖类 /
- 枯否细胞 /
- 综述
Abstract: Endotoxin,which is also called lipopolysaccharide( LPS),is a unique element of Gram- negative bacteria. Liver is the main site for removing bacteria and endotoxin. Meanwhile,it is also the most vulnerable organ. Liver injury initially occurs in the hepatic sinusoids. This article mainly introduces the impact of LPS on Kupffer cells,hepatic sinusoidal endothelial cells,oxidant / antioxidant balance in the hepatic sinusoids,and liver blood flow. It is believed that the function of hepatic sinusoids in LPS- induced liver injury should not be ignored,and the hepatic sinusoids would play an important role in the prevention and treatment of LPS- induced liver injury.
- liver diseases /
- lipopolysaccharides /
- kupffer cells /
- review

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参考文献(31)

[1]SCHNABL B,BRENNER DA.Interactions between the intestinal microbiome and liver diseases[J].Gastroenterology,2014,146(6):1513-1524.

[2]QI HY,XIAO HL,YIN CH,et al.The characteristics and mechanism in acute liver damange cause by endotoxinemia[J].Chin J Integr Tradit Chin West Med Intensive Crit Care,2014,21(2):144-146.(in Chinese)齐海宇,肖红丽,阴赪宏,等.内毒素血症急性肝损伤的特点及致病机制[J].中国中西医结合急救杂志,2014,21(2):144-146.

[3]KREIDER BQ,MESSING A,DOAN H,et al.Enrichment of Schwann cell cultures from neonatal rat sciatic nerve by differential adhesion[J].Brain Res,1981,207(2):433-444.

[4]CHELUVAPPA R,DENNING GM,LAU GW,et al.Pathogenesis of the hyperlipidemia of Gram-negative bacterial sepsis may involve pathomorphological changes in liver sinusoidal endothelial cells[J].Int J Infect Dis,2010,14(10):e857-e867.

[5]QIU DK,HUA J,LI JQ,et al.CD14 expression on Kupffer cells during the course of carbon tetrachloride-mediated liver injury[J].Chin J Dig Dis,2005,6(3):137-141.

[6]SCHULZ C,GOMEZ PERDIGUERO E,CHORRO L,et al.A lineage of myeloid cells independent of Myb and hematopoietic stem cells[J].Science,2012,336(6077):86-90.

[7]FITZGERALD KA,ROWE DC,GOLENBOCK DT.Endotoxin recognition and signal transduction by the TLR4/MD2-complex[J].Microbes Infect,2004,6(15):1361-1367.

[8]TRACY TF JR,FOX ES.CD14-lipopolysaccharide receptor activity in hepatic macrophages after cholestatic liver injury[J].Surgery,1995,118(2):371-377.

[9]HAN DW.Intestinal endotoxemia as a pathogenetic mechanism in liver failure[J].World J Gastroenterol,2002,8(6):961-965.

[10]MINTER RM,FAN MH,SUN J,et al.Altered Kupffer cell function in biliary obstruction[J].Surgery,2005,138(2):236-245.

[11]ZHANG H,ZHAO C,LI X,et al.Study of monocyte membrane proteome perturbation during lipopolysaccharide-induced tolerance using iT RAQ-based quantitative proteomic approach[J].Proteomics,2010,10(15):2780-2789.

[12]OZMENT TR,HA T,BREUEL KF,et al.Scavenger receptor class a plays a central role in mediating mortality and the development of the pro-inflammatory phenotype in polymicrobial sepsis[J].PLoS Pathog,2012,8(10):e1002967.

[13]PLUDDEMANN A,NEYEN C,GORDON S.Macrophage scavenger receptors and host-derived ligands[J].Methods,2007,43(3):207-217.

[14]VERBEKE L,NEVENS F,LALEMAN W.Bench-to-beside review:acute-on-chronic liver failure-linking the gut,liver and systemic circulation[J].Crit Care,2011,15(5):233.

[15]SHANAHAN F.Physiological basis for novel drug therapies used to treat the inflammatory bowel diseases I.Pathophysiological basis and prospects for probiotic therapy in inflammatory bowel disease[J].Am J Physiol Gastrointest Liver Physiol,2005,288(3):g417-g421.

[16]WU J,ZHANG YY,GUO L,et al.Bupleurum polysaccharides attenuates lipopolysaccharide-induced inflammation via modulating Toll-like receptor 4 signaling[J].PLoS One,2013,8(10):e78051.

[17]ISHIZAKI-KOIZUMI S,SONAKA I,TAKEI Y,et al.The glycine analogue,aminomethanesulfonic acid,inhibits LPS-induced production of TNF-alpha in isolated rat Kupffer cells and exerts hepatoprotective effects in mice[J].Biochem Biophys Res Commun,2004,322(2):514-519.

[18]TSUTSUI H,NISHIGUCHI S.Importance of Kupffer cells in the development of acute liver injuries in mice[J].Int J Mol Sci,2014,15(5):7711-7730.

[19]RIORDAN SM,SKINNER NA,KURTOVIC J,et al.Toll-like receptor expression in chronic hepatitis C:correlation with pro-inflammatory cytokine levels and liver injury[J].Inflamm Res,2006,55(7):279-285.

[20]WAN JM,SIT WH,LEE CL,et al.Protection of lethal toxicity of endotoxin by Salvia miltiorrhiza BUNGE is via reduction in tumor necrosis factor alpha release and liver injury[J].Int Immunopharmacol,2006,6(5):750-758.

[21]LAPEYRE-MESTRE M,de CASTRO AM,BAREILLE MP,et al.Non-steroidal anti-inflammatory drug-related hepatic damage in France and Spain:analysis from national spontaneous reporting systems[J].Fundam Clin Pharmacol,2006,20(4):391-395.

[22]WATANABE T,JONO H,HAN J,et al.Synergistic activation of NF-kappaB by nontypeable Haemophilus influenzae and tumor necrosis factor alpha[J].Proc Natl Acad Sci U S A,2004,101(10):3563-3568.

[23]IMAMURA M,TSUTSUI H,YASUDA K,et al.Contribution of TIR domain-containing adapter inducing IFN-β-mediated IL-18 release to LPS-induced liver injury in mice[J].J Hepatol,2009,51(2):333-341.

[24]BOSSALLER L,CHIANG PI,SCHMIDT-LAUBER C,et al.Cutting edge:FAS(CD95)mediates noncanonical IL-1βand IL-18maturation via caspase-8 in an RIP3-independent manner[J].J Immunol,2012,189(12):5508-5512.

[25]SPOLARICS Z.Endotoxemia,pentose cycle,and the oxidant/antioxidant balance in the hepatic sinusoid[J].J Leukoc Biol,1998,63(5):534-541.

[26]CHEN FJ,XU JQ,SONG BY,et al.Study of the mechanism of lipopolysaccharide on the expression of connective tissue growth factor in primary hepatic stellate cells of rats[J].China Med Herald,2013,10(14):15-17.(in Chinese)陈峰杰,徐军全,宋彬妤,等.内毒素对原代大鼠肝星状细胞表达结缔组织生长因子影响机制的研究[J].中国医药导报,2013,10(14):15-17.

[27]KAWA K,TSUTSUI H,UCHIYAMA R,et al.IFN-gamma is a master regulator of endotoxin shock syndrome in mice primed with heat-killed Propionibacterium acnes[J].Int Immunol,2010,22(3):157-166.

[28] YOU HB,GONG JP.Mechanism of endotoxin induced in hepatic injury[J].Chin J Med Writ,2005,12(5):431-434.(in Chinese)游海波,龚建平.内毒素致肝损伤的机制[J].中华医学写作杂志,2005,12(5):431-434.

[29]TAYLOR DE,GHIO AJ,PIANTADOSI CA.Reactive oxygen species produced by liver mitochondria of rats in sepsis[J].Arch Biochem Biophys,1995,316(1):70-76.

[30]CHEN L,LI QY,WU JK.Progress in the pathogenesis of liver injury in spesis[J].Med Recapitulate,2014,20(19):3529-3531.(in Chinese)陈琳,厉其昀,吴家宽.脓毒症肝损伤发生机制研究进展[J].医学综述,2014,20(19):3529-3531.

[31]HUTCHINS NA,CHUNG CS,BORGERDING JN,et al.Kupffer cells protect liver sinusoidal endothelial cells from Fas-dependent apoptosis in sepsis by down-regulating gp130[J].Am J Pathol,2013,182(3):742-754.

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