非诺贝特对胆管结扎大鼠血生化及肝组织病理学的影响

王一波; 刘阳; 孙运涛

非诺贝特对胆管结扎大鼠血生化及肝组织病理学的影响

1. 济宁医学院附属医院
2. 山东大学医学院

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中图分类号: R965
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出版历程
- 出版日期: 2011-09-20

Effect of fenofibrate on serum biochemical indicators and hepatic pathology in rats after bile duct ligation

摘要

摘要: 目的探讨非诺贝特对胆管结扎大鼠血清肝脏生化指标、肝组织丙二醛含量及组织病理学的影响。方法采用胆总管结扎手术制备胆汁淤积大鼠模型。24只雄性W istar大鼠随机分为两组（每组12只）:A组为胆管结扎+生理盐水组,B组为胆管结扎+非诺贝特组（30 mg/kg）。术后7 d留取血标本及肝组织后处死。采用全自动生化分析仪检测肝脏生化指标;分光光度计检测肝组织丙二醛含量;光镜下观察肝脏组织病理变化。结果两组血清肝脏生化指标无显著统计学意义;B组大鼠肝组织MDA含量显著低于A组（P=0.001）;B组肝脏坏死面积较A组显著减轻（P<0.05）,汇管区小胆管数目较A组明显减少（P<0.05）。结论非诺贝特可显著降低MDA含量,减少肝脏坏死面积以及小胆管增生。
- 普鲁脂芬 /
- 黄疸,阻塞性 /
- 疾病模型,动物 /
- 血液化学分析
Abstract: Objective To investigate the effect of Fenofibrate on serum hepatic biochemical indicators、MDA (malonaldehyde) and hepatic pathology in rats after bile duct ligation.Methods Rats were subjected to bile duct ligation to establish the cholestasis model.Twenty-four male Wistar rats were randomly divided into two groups equally: A = bile duct ligation+normal saline (BDL + NS) , B= BDL + fenofibrate (30 mg/kg daily) .All rats were sacrificed on 7th day after obtaining blood samples and liver tissue.Serum hepatic biochemical indicators were detected with automatic biochemistry analyzer;MDA assays were performed by spectrophotometer;Histopathological changes in liver was dyed with HE and observed under light microscope.Results There was no significant difference in terms of serum hepatic biochemical levels between group A and group B;The levels of MDA in rats of group B were significantly lower than in group A (P=0.001<0.05) ;The number of liver necrotic area in rats of group B was significantly smaller than in group A (P<0.05) , The number of biliary canals in rats of group B was significantly smaller than in group A (P<0.05) .Conclusion Fenofibrate administration attenuates the levels of MDA, reduces liver necrotic area and ductular proliferation.
- procetofen /
- jaundice /
- obstructive /
- disease models

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参考文献(16)

[1]许海波, 巩鹏.PPARs在梗阻性黄疸肝脏损伤中的作用[J].国际外科学杂志, 2007, 34 (7) , 461-465.

[2]Cindoruk M, Kerem M, Karakan T, et al.Peroxisome prolif-erators-activated alphaagonist treatment ameliorates hepat-ic damage in rats with obstructive jaundice:an experimentalstudy[J].BMC Gastroenterology, 2007, 7 (44) :1-7.

[3]Lalloyer F, Staels B.Fibrates, glitazones, and peroxisomeproliferator-activated receptors[J].Arterioscler ThrombVasc Biol, 2010, 30 (5) :894-899.

[4]Post SM, Duez H, Gervois PP, et al.Fibrates suppress bileacid synthesis viaperoxisome proliferator-activated receptor-alpha-mediated downregulation of cholesterol 7alpha-hydroxylase and sterol27-hydroxylase expression[J].Arte-rioscler Thromb Vasc Biol, 2001, 21 (11) :1840-1845.

[5]Zollner G, Trauner M.Nuclear receptors as therapeutic tar-gets in cholestatic liver diseases[J].Br J Pharmacol, 2009, 156 (1) :7-27.

[6]Trauner M, Meierer PJ, Boyer JL.Molecular pathogenesisof cholestasis[J].New Eng J Med, 1998, 339 (17) :1217-1227.

[7]Aller MA, Arias JL, Prieto I, et al.Bile duct ligation:step-by-step to cholangiocyte inflammatory tumorigenesis[J].Eur J Gastroenterol Hepatol, 2010, 22 (6) :651-661.

[8]Reddy JK, Hashimoto T.Peroxisomal beta-oxidation andperoxisome proliferator-activated receptor alpha:an adap-tive metabolic system[J].Annu Rev Nutr, 2001, 21:193-230.

[9]Qi C, Zhu Y, Reddy JK.Peroxisome proliferator-activatedreceptors, coactivators, and downstream targets[J].CellBio-chem Biophys, 2000, 32:187-204.

[10]Bulhak AA, Jung C, Ostenson CG, et al.PPAR-alpha acti-vation protects the type 2 diabetic myocardium against ische-mia-reperfusion injury:involvement of the PI3-Kinase/Aktand NO pathway[J].Am J Physiol Heart Circ Physiol, 2009, 296 (3) :H719-H727.

[11]Collino M, Aragno M, Mastrocola R, et al.Oxidative stressand inflammatory response evoked by transient cerebral is-chemia reperfusion:effects of the PPAR-alpha agonistWY14643[J].Free Radic Biol Med, 2006, 41 (4) :579-589.

[12]曲艳萍, 张文锐.浅谈非诺贝特的副作用[J].中外医疗, 2010, 2 (29) :176-176.

[13]Kobayashi A, Suzuki Y, Kuno H, et al.Effects of fenofibrateon plasma and hepatic transaminase activities and hepatictransaminase gene expression in rats[J].J Toxicol Sci, 2009, 34 (4) :377-387.

[14]Tomkiewicz C, Muzeau F, Edgar AD, et al.Opposite regula-tion of the rat and human cytosolic aspartate aminotrans-ferase genes by fibrates[J].Biochem Pharmacol, 2004, 67 (2) :213-225.

[15]尹蓉, 王沁, 富翠芹.姜黄素对酒精诱导的大鼠脂质过氧化反应的影响[J].世界华人消化杂志, 2008, 16 (13) :1383-1387.

[16]Tolman KG.Defining patient risks from expanded preventivetherapies[J].Am J Cardiol, 2000, 85 (12A) :15E-19E.

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