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Protective effect of polyunsaturated phosphatidylcholine on liver damage induced by biliary obstruction in rats.

机译:多不饱和磷脂酰胆碱对大鼠胆道梗阻所致肝损伤的保护作用。

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摘要

BACKGROUND/PURPOSE: Persistent inflammatory response secondary to congenital or acquired biliary choleastasis plays an important role in the pathophysiology of hepatic tissue damage. The polyunsaturated fatty acids (PUFA) have been shown to suppress the inflammatory reactions in vivo and in vitro. PUFA has been shown also to protect against various types of experimental liver damage in animal models and isolated hepatocytes. Therefore, the aim of this study was to investigate the protective effect of PUFA administration on liver damage using the rat chronic biliary obstruction model. METHODS: Swiss albino rats of either sex were divided into 4 groups as follows: control group (group 1, 10 rats); rats with sham operation and treated with saline group 2, 10 rats); rats with biliary obstruction (group 3, 15 rats); and polyunsaturated phophatidylcholine (PPC)-treated rats with biliary obstruction (Group 4, 15 rats). Biliary obstruction was induced by double ligation and division of the common bile duct. PUFA treatment was started 2 weeks later from biliary obstruction in doses of 50 mg/d per rat and continued for 2 weeks. All animals were killed after 4 weeks of common bile duct ligation or sham operation. Liver damage and cholestasis were determined by biochemical and histologic examinations. RESULTS: The data showed a decrease in plasma bilirubin level (both conjugated and unconjugated) and liver enzyme levels (AST, ALT, AP, GGT, 5'-NT) in group 4, when compared with group 3 (P <.05). Tissue levels of malondialdehyde (MDA) in group 4 was 20.00 +/- 2.93 compared with that in group 3, 27.12 +/- 2.96 (P <.05). Administration of PUFA to the biliary obstructed rats resulted in inhibition of collagen accumulation (P <.05) and ductal proliferation (P <.05). CONCLUSIONS: PUFA reduced liver damage, ductular proliferation, and fibrosis in biliary obstructed rats. These effects suggest that it might be a useful agent to preserve liver function in patients with biliary obstruction such as biliary atresia.
机译:背景/目的:先天性或获得性胆汁性胆汁淤积性继发的持续性炎症反应在肝组织损伤的病理生理中起重要作用。已显示多不饱和脂肪酸(PUFA)在体内和体外抑制炎症反应。在动物模型和分离的肝细胞中,PUFA还被证明可以防止各种类型的实验性肝损伤。因此,本研究的目的是使用大鼠慢性胆道梗阻模型研究PUFA给药对肝损伤的保护作用。方法:将瑞士的两性白化病大鼠分为4组,分别为:对照组(第1组,每组10只)。假手术大鼠,加生理盐水2组,每只10只。胆道梗阻大鼠(第3组,每组15只);和多不饱和磷脂酰胆碱(PPC)治疗的胆道梗阻大鼠(第4组,15只大鼠)。胆总管的双重结扎和分裂引起胆道梗阻。胆道阻塞后2周开始以每只大鼠50 mg / d的剂量开始PUFA治疗,并持续2周。胆总管结扎或假手术4周后杀死所有动物。通过生化和组织学检查确定肝损害和胆汁淤积。结果:与第3组相比,数据显示第4组血浆胆红素水平(结合和未结合)和肝酶水平(AST,ALT,AP,GGT,5'-NT)降低(P <.05) 。第4组的丙二醛(MDA)组织水平为20.00 +/- 2.93,而第3组的组织水平为27.12 +/- 2.96(P <.05)。胆道梗阻大鼠给予PUFA会抑制胶原蛋白的积累(P <.05)和导管增生(P <.05)。结论:PUFA减轻了胆道梗阻大鼠的肝损伤,导管增生和纤维化。这些效果表明,它可能是保持胆道梗阻(如胆道闭锁)患者肝功能的有用药物。

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