Objective To explore the effect of cell apoptosis and oxidative stress on stressive liv-er injury after traumatic brain injury (TBI) in rats. Methods The model of TBI was duplicated by u-sing modified Allen's mehtods. Forty male Wistar rats were randomly divided into control group and groups at 6,12,24,48 hours after TBI. The serum levels of ALT and AST as well as the levels of superox-ide dismutase (SOD) and malandialdehyde in liver tissue were measured. The index of hepatocyte apopto-sis was detected through flow cytometer. Pathological changes of liver tissues were observed under light and electron microscopes. Results After TBI, the serum levels of ALT and AST were significantly in-creased, while malondialdehyde was increased and SOD decreased in liver tissues. The electron micro-scope showed that the index of hepatocyte apoptosis reached a peak at 6 hours after TBi. Aggressive inju-ries of the liver tissues were observed after TBI, showed by pathological observations. Conclusion Cell apoptosis and oxidative stress may be involved in the pathogenesis of stressive liver injury after TBI.