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1 Introduction As a subtype of hepatic encephalopathy, acute hepatic encephalopathy (AHE) is characterized by severe neurological disorder caused by acute liver injury, with a mortality rate exceeding 80% ( + level in mitochondria, triggering redox imbalance and enhancing reactive oxygen species production (ROS) ( An increasing number of studies in recent years have consistently identified HE as the most prevalent complication of liver cirrhosis, significantly impacting quality of life, incidence rate, and mortality, thereby exacerbating the medical burden ( Salmonella meningitis ( Therefore, this study systematically explored the therapeutic potential of exogenous GSH in thioacetamide (TAA)-induced AHE model rats, affirming the feasibility of GSH as a therapeutic agent for AHE through investigations into its pharmacokinetics and molecular mechanisms of AHE treatment

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