Márquez-Aguirre A L, Canales-Aguirre A A, Gómez-Pinedo U, Gálvez-Gastélum F J
Unidad de Biotecnología Médica y Farmacéutica, Centro de Investigación y Asistencia en Tecnología y Diseño del Estado de Jalisco, CIATEJ, Guadalajara, México.
Neurologia. 2010 May;25(4):239-47.
Liver fibrosis and its end stage, cirrhosis, is an enormous worldwide health problem. Hepatic encephalopathy (HE) or portal-systemic encephalopathy continues to be a major clinical problem of long-term cirrhosis. In this review we emphasise the molecular basis of HE and the involvement of oxidative stress in the development of this disease.
Several studies suggest that the pathogenesis of HE could be multifactorial and have implicated different factors, such as alterations in blood brain barrier, substances; such as ammonia and manganese, neurotransmission disorders such as dopamine, glutamate and GABA.
HE is a severe complication of both acute and chronic liver failure. Neuropathologically, it is characterized by astrocyte changes known as Alzheimer type II astrocytosis. In addition, astrocytes manifest altered expression of astrocyte-specific proteins, such as, glial fibrillary acidic protein, glutamine synthetase, monoamine oxidase and peripheral type benzodiazepine receptors.
HE is a complex neuropsychiatric syndrome associated with liver failure. These alterations are products of increases in oxidative stress in brain due to neurotoxin activity. The main strategy for HE treatment is directed at ammonia reduction, which can be achieved either by decreasing its absorption/production or increasing its removal.
肝纤维化及其终末期肝硬化是一个全球性的重大健康问题。肝性脑病（HE）或门体性脑病仍然是长期肝硬化的主要临床问题。在本综述中，我们强调了HE的分子基础以及氧化应激在该疾病发展过程中的作用。
多项研究表明，HE的发病机制可能是多因素的，涉及不同的因素，如血脑屏障的改变、物质（如氨和锰）、神经传递紊乱（如多巴胺、谷氨酸和γ-氨基丁酸）。
HE是急性和慢性肝衰竭的严重并发症。在神经病理学上，其特征是出现称为阿尔茨海默II型星形细胞增生的星形细胞变化。此外，星形细胞表现出星形细胞特异性蛋白（如胶质纤维酸性蛋白、谷氨酰胺合成酶、单胺氧化酶和外周型苯二氮䓬受体）表达的改变。
HE是一种与肝衰竭相关的复杂神经精神综合征。这些改变是由于神经毒素活性导致脑内氧化应激增加的产物。HE治疗的主要策略是针对降低氨水平，这可以通过减少其吸收/产生或增加其清除来实现。
