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研究提示,原发性胆汁性肝硬化的肝损害是由于毒性疏水性胆汁酸滞留所致,而亲水性熊脱氧胆酸(UDCA)的治疗作用就是减轻这种损害。UDCA并可降低特异性线粒体酶和抗线粒体抗体的血清值。但有关线粒体受损和保护机制仍不清。本文目的为检测疏水性和亲水性胆汁酸对人肝细胞线粒体结构和功能的影响。 对取自无肝病病人的楔形肝活检作蔗糖梯度超速离心以制备线粒体。为检测结构性影响,用鹅脱氧胆酸(CDCA)和UDCA0～10mM测定线粒体蛋白溶解性,并通过测定琥珀酸细胞色素C还原酶研究线粒体电子转换,以评估功能性影响。在0:5mM胆汁酸
Studies suggest that liver damage in primary biliary cirrhosis is due to retention of toxic hydrophobic bile acids, and that the therapeutic effect of hydrophilic ursodeoxycholic acid (UDCA) is to reduce this damage. UDCA also reduces serum levels of specific mitochondrial enzymes and anti-mitochondrial antibodies. However, the mechanism of mitochondrial damage and protection remains unclear. The purpose of this paper is to examine the effect of hydrophobic and hydrophilic bile acids on the mitochondrial structure and function of human hepatocytes. Mitochondria were prepared by sucrose gradient ultracentrifugation on wedge-shaped liver biopsies from patients without liver disease. To test for structural effects, mitochondrial protein solubility was determined using chenodeoxycholic acid (CDCA) and UDCA 0-10 mM and mitochondrial electron transitions were studied by measuring succinate cytochrome C reductase to assess functional effects. At 0: 5 mM bile acid