Acute stress disorder（ ASD） is a common acute psychological response after traumatic exposure， and some patients may progress to post-traumatic stress disorder. Early identification and intervention have significant clinical significance. Traumatic stress not only involves abnormal responses in the central nervous system but also affects hepatic metabolic rhythms and gut microbiota homeostasis through the hypothalamic-pituitary-adrenal axis， autonomic nervous system， and circadian rhythm regulatory pathways. At the same time， alterations in gut microbiota composition， as well as hepatic metabolic and inflammatory signals， can also feedback regulate brain function， which is associated with the formation of ASD symptom phenotypes and disease progression. The ratio of Firmicutes to Bacteroides in the gut microbiota exhibits stress type specific changes. Dysregulation of the hepatic clock gene nuclear receptor subfamily 1 group D member 1（ REV-ERBα）， may exacerbate liver-gut dysfunction through bile acid synthesis and lipid metabolism pathways， and interfere with central stress regulation. The liver-gut-brain axis provides a mechanistic framework for explaining the coupling mechanisms between central and peripheral stress responses in ASD. This review summarizes recent advances in ASD research through the lens of the liver-gut-brain axis. It specifically highlights REV-ERBα mediated metabolic rhythm disruption， gut dysbiosis， and neuroimmune effects， aiming to offer novel insights into underlying mechanisms and targeted therapeutic interventions.