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Abstract：
Hepatic encephalopathy (HE) following acute and chronic liver failure is defined as a complex of neuropsychiatric abnormalities, such as discrete personal changes, sleep disorder, forgetfulness, confusion, and decreasing the level of consciousness to coma. The use and design of suitable animal models that represent clinical features and pathological changes of HE are valuable to map the molecular mechanisms that result in HE. Among different types of animal models, thioacetamide (TAA) has been used extensively for the induction of acute liver injury and HE. This agent is not directly hepatotoxic but its metabolites induce liver injury through the induction of oxidative stress and produce systemic inflammation similar to that seen in acute HE patients. In this short review article, we shortly review the most important pathological findings in animal models of acute HE following the administration of TAA.
摘要：
急性和慢性肝衰竭后的肝性脑病（HE）被定义为神经精神异常的复合物，例如离散的个人变化，睡眠障碍,健忘,混乱,并降低昏迷的意识水平。代表HE的临床特征和病理变化的合适动物模型的使用和设计对于绘制导致HE的分子机制是有价值的。在不同类型的动物模型中，硫代乙酰胺（TAA）已广泛用于诱导急性肝损伤和HE。这种药物不是直接的肝毒性，但其代谢物通过诱导氧化应激诱导肝损伤，并产生类似于急性HE患者的全身性炎症。在这篇简短的评论文章中，我们简要回顾了TAA给药后急性HE动物模型中最重要的病理发现。
