Abstract: As the most widely used antipyretic analgesic, acetaminophen has been widely used as a model drug to study mechanisms of chemical-induced liver toxicity and test hepato-protective potential of new drugs. Inflammation may aggravate cell damage, by limiting cell injury, removing cell debris and promoting regeneration. The mechanisms of AAP-induced liver cell injury have been extensively investigated and discussed for more than 30 years. This review focuses on the intracellular events of acetaminophen-induced hepatotoxicity, particularly the relevance of the inflammatory response, inflammatory mediators and inflammatory cells, to help improve clinical application and lay a good basis for mechanism investigation.