Role and action mechanism of 8-iso-PGF2α in traumatic liver diseases
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摘要: 活性氧自由基引发的氧化应激主要通过启动膜脂质过氧化反应改变生物膜的功能,并在一系列细胞因子的共同作用下引起不同程度的肝损害。8-iso-PGF2α是脂质过氧化反应的特异性产物,具有很强的生物学活性,目前被认为是评价氧化应激和脂质过氧化损伤的金指标。文章简述了损伤性肝脏疾病与脂质过氧化的关系,并提出以8-iso-PGF2α作为肝脏疾病过氧化损伤程度的敏感指标,初步探讨了其在肝脏疾病中的应用前景。Abstract: Oxidative stress caused by reactive oxygen species changes the function of biofilm mainly by initiating membrane lipid peroxidation and causes varying degrees of liver damage along with a series of cytokines. As the specific product of lipid peroxidation, 8-iso-PGF2α has strong bioactivity and is currently considered the gold indicator for evaluating oxidative stress and lipid peroxidation damage. The relationship between traumatic liver diseases and lipid peroxidation is summarized; 8-iso-PGF2α is recommended as a sensitive indicator of peroxidative damage in liver diseases, and its potential use in liver diseases is preliminarily discussed.
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Key words:
- dinoprost /
- 8-iso-PGF2 alpha /
- lipid peroxidation /
- liver diseases
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[1]MURIEL P.Role of free radicals in liver diseases[J].Hepatol Int, 2009, 3 (4) :526-536. [2]MEZZETTI A, CIPOLLONE F, CUCCURULLO F.Oxidative stress and cardiovascular complications in diabetes:isoprostanes as new markers on an old paradigm[J].Cardiovasc Res, 2000, 47 (3) :475-488. [3]YANG LL, LIU T, WANG M, et al.Oxidative stress and non-alcoholic fatty liver disease research progress[J].World Chin J Digestol, 2009, 17 (9) :896-900. (in Chinese) 杨丽丽, 柳涛, 王淼, 等.氧化应激与非酒精性脂肪性肝病研究进展[J].世界华人消化杂志, 2009, 17 (9) :896-900. [4]KUMAR A, KINQDON E, NORMAN J, et al.The isoprostane 8-iso-PGF2 alpha suppresses monocyte adhesion to human microvascular endothelial cells via two independent mechanisms[J].FASEB J, 2005, 19 (3) :443-445. [5]WANG X, CEDERBAUM AI.Acute ethanol pretreatment increase FAS-mediated liver injury in mice role of oxidative stress and CYP2E1-dependent and independent pathway[J].Free Radic Biol Med, 2007, 42 (7) :971-984. [6]WANG X, ENO CO, ALTMAN BJ, et al.ERstress modulates cellular metabolism[J].Biochem J, 2011, 435 (1) :285-296. [7]YANG BZ, REN F, DUAN ZP, et al.Endoplasmic reticulum stress and viral hepatitis[J].Chin J Gastroenterol Hepatol, 2013, 22 (2) :167-170. (in Chinese) 杨丙章, 任锋, 段钟平, 等.内质网应激与病毒性肝炎[J].胃肠病学和肝病学杂志, 2013, 22 (2) :167-170. [8]FENG LJ, SHEN YX, LI J.Endoplasmic reticulum stress and inflammation[J].Chin Pharmacol Bull, 2013, 29 (6) :756-760. (in Chinese) 冯利杰, 沈玉先, 李俊.内质网应激与炎症[J].中国药理学通报, 2013, 29 (6) :756-760. [9]CHOI J, OU JH.Mechanism of liver injury.Ⅲ.Oxidative stress in the pathogenesis of hepatitis C virus[J].Am J Physiol Gastrointest Liver Physiol, 2006, 290:g847-g851. [10]JOYCE MA, WALTERS KA, LAMB SE, et al.HCV induces oxidative and ER stress, and sensitize infected cells to apoptosis in SCID/AlbuPA mice[J].PLoS Pathog, 2009, 5 (2) :e1000291. [11]CHRISTEN V, TREVES S, DUONG FH, et al.Activation of endoplasmic reticulum stress response by hepatitis viruses up-regulates protein phosphatase 2A[J].Hepatology, 2007, 46 (2) :558-565. [12]MENG XB.Patients withchronic hepatitis B SF, serum IGF-Ilevels and the relationship between lipid peroxidation[J].J Radioimmunol, 2011, 24 (2) :133-135. (in Chinese) 孟晓波.慢性乙型肝炎患者SF、血清IGF-I水平与脂质过氧化损伤的关系[J].放射免疫学杂志, 2011, 24 (2) :133-135. [13]LEE UE, FRIEDMAN SL.Mechanisms of hepatic fibrogenesis[J].Best Pract Res Clin Gastroenterol, 2011, 25 (2) :195-206. [14]MANNAERTS I, NUYTTEN NR, ROGIERS V, et al.Chronic administration of valproic acid inhibits activation of mouse hepatic stellate cells in vitro and in vivo[J].Hepatology, 2010, 51 (2) :603-614. [15]WANG J, LECLERCQ I, BRYMORA JM, et al.Kupffer cells mediate leptin induced liver fibrosis[J].Gastroenterology, 2009, 137 (7) :713-723. [16]BRUNATI AM, PAGANO MA, BINDOLI A, et al.Thiol redox systems and protein kinases in hepatic stellate cell regulatory processes[J].Free Radic Res, 2010, 44 (4) :363-378. [17]ZHU BH, ZHANG HF, CHEN YP.TGF-1 in rat liver fibrosis tissue research[J].Chin J Microecol, 2013, 25 (2) :150-152. (in Chinese) 朱碧红, 张慧芳, 陈永平.大鼠肝纤维化组织中TGF-1的研究[J].中国微生态学杂志, 2013, 25 (2) :150-152. [18]STARKEL P, SEMPOUX C, LECLERCQ I, et al.Oxidative stress, KLF6 and transforming growth factor-beta up-regulation differentiate non-alcoholic steatohepatitis progressing to fibrosis from uncomplicated steatosis in rats[J].J Hepatol, 2003, 39 (4) :538-546. [19]ZHANG LF, WEI W, XU JM, et al.Inhibitory effect of melatonin on diquat-induced lipid peroxidation in vivo as assessed by the measurement of F2-isoprostanes[J].Pineal Res, 2006, 40 (4) :326-331. [20]COMPORTI M, AREZZINI B, SIGNORINI C, et al.F2-isoprostanes stimulate collagen synthesis in activated hepatic stellate cells:a link with liver fibrosis?[J].Lab Invest, 2005, 85 (11) :1381-1391. [21]FANG L, DU SY, ZHAO HC, et al.Role of oxidative stress in the pathogenesis of chronic hepatic injury induced by ethanol and carbon tetrachloride in rats[J].World Chin J Digestol, 2010, 18 (3) :234-239. [22]ZHU H, JIA Z, MISRA H, et al.Oxidative stress and redox signaling mechanisms of alcoholic liver disease:Updated experimental and clinical evidence[J].J Dig Dis, 2012, 13 (3) :133-142. [23]LAMLE J, MARHENKE S, BORLAK J, et al.Nuclear factor-eythroid2-related factor 2 prevents alcohol-induced fulminant liver injury[J].Gastroenterology, 2008, 134 (4) :1159-1168. [24]KLAASSEN CD, REISMAN SA.Nrf2 the rescue:effects of the antioxidative/electrophilic response on the liver[J].Toxicol Appl Pharmacol, 2010, 244 (1) :57-65. [25]PESSAYRE D.Role of mitochondria in non-alcoholic fatty liver disease[J].J Gastroenterol Hepatol, 2007, 22 (Suppl 1) :s20-s27. [26]LIU Y, LI CP.The role of oxygen stress and lipid peroxidation and liver cell apoptosis in nonalcoholic fatty liver disease[J].Southwest Med, 2008, 10 (4) :3-6. (in Chinese) 刘翼, 李昌平.氧应激、脂质过氧化及肝细胞凋亡在非酒精性脂肪肝病中的作用[J].西南军医, 2008, 10 (4) :3-6.
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