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.
Keywords: ALT, alanine aminotransferase; AQP4, aquaporin 4 water channel; AST, aspartate aminotransferase; Acute liver failure; Animal model; B7, B7 molecules (CD80+CD86); BBB, blood-brain barrier; CBF, cerebral blood flow; CCL2, chemokine ligand 2; CNS, central nervous system; CTLA4, Cytotoxic T-lymphocyte-associated Protein 4; CYP2E1, Cytochrome P450 family 2 subfamily E member 1; GFAP, glial fibrillary acidic protein; HE, hepatic encephalopathy; Hepatic encephalopathy; IL-6, interleukin 6; IL-β, interleukin 1 β; Iba1, ionized calcium-binding adaptor molecule 1; JNK, c-Jun N-terminal kinase; NAC, N-acetylcysteine; NF-κB, nuclear factor κB; OA, L-ornithine-l-aspartate; ROS, reactive oxygen species; TAA, thioacetamide; TASO, thioacetamide sulfoxide; TASO2, thioacetamide sulfdioxide; TLR-2, toll-like receptor 2; TLR-4, toll-like receptor 4; TNFα, tumor necrosis factor α; Thioacetamide; Toxicity pathway.
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