To figure out the pathogenesis of HE, the improvement of the animal model is warranted.
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TAA has been introduced as a valid model because it mimics many pathological features of patients with ALF and HE.
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TAA as a chemical agent leads to liver injury by triggering the production of ROS and proinflammatory cytokines.
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TAA causes impairment of CBF, gliopathy, neuroinflammation, and neurological impairments that are seen in ALF patients.
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.
