Grattagliano Ignazio, Calamita Giuseppe, Cocco Tiziana, Wang David Q-H, Portincasa Piero
Ignazio Grattagliano, Italian College of General Practitioners, 50100 Florence, Bari 70124, Italy.
World J Gastroenterol. 2014 May 21;20(19):5746-59. doi: 10.3748/wjg.v20.i19.5746.
Primary biliary cirrhosis is a multifactor autoimmune disease characterized by hepatic and systemic manifestations, with immune system dysregulation and abnormalities in the hepatic metabolism of bile salts, lipids, and nutrients, as well as destruction of membrane lipids and mitochondrial dysfunction. Both oxidative and nitrosative stress are associated with ongoing manifestations of the disease. In particular, abnormalities in nitric oxide metabolism and thiol oxidation already occur at early stages, thus leading to the hypothesis that these biochemical events play a pathogenic role in primary biliary cirrhosis. Moreover, the association of these metabolic abnormalities with the progression of the disease may indicate some biochemical parameters as early diagnostic markers of disease evolution, and may open up the potential for pharmacological intervention to inhibit intra- and extra-cellular stress events for resuming hepatocellular functions. The following paragraphs summarize the current knowledge by outlining molecular mechanisms of the disease related to these stress events.
原发性胆汁性肝硬化是一种多因素自身免疫性疾病,其特征为肝脏和全身表现,伴有免疫系统失调以及胆汁盐、脂质和营养物质的肝脏代谢异常,同时存在膜脂质破坏和线粒体功能障碍。氧化应激和亚硝化应激均与该疾病的持续表现相关。特别是,一氧化氮代谢和硫醇氧化异常在疾病早期就已出现,因此产生了这些生化事件在原发性胆汁性肝硬化中起致病作用的假说。此外,这些代谢异常与疾病进展的关联可能表明某些生化参数可作为疾病进展的早期诊断标志物,并可能为通过抑制细胞内和细胞外应激事件来恢复肝细胞功能的药物干预开辟潜力。以下段落通过概述与这些应激事件相关的疾病分子机制来总结当前的知识。