Aim To study the activation of Nrf2 in-duced by baicalein ( BAI ) , and its protection against carbon tetrachloride ( CCl4 ) , ethanol and acetamino-phen ( APAP )-induced hepatotoxicity. Methods A reporter gene assay was conducted in human normal liver L-02 cells to detect the activation of transcription factor Nrf2 induced by baicalein. APAP ( 10 mmol · L-1 ) , CCl4 (10 mmol·L-1 ) and Ethanol (100 mmol · L-1 ) were used to induce hepatotoxicity in L-02 cells. After the pre-incubation with Baicalein (0, 1, 10, 25, 50, 100 μmol·L-1 ) for 15 min, cells were administrated with or without those above hepatotoxins. 48 h later, cell viability was detected by 3-(4, 5-dim-ethylthiazol-2-yl ) 2 , 5-diphenyltetrazolium bromide (MTT) method. Results Baicalein (25, 50 μmol· L-1 ) induced the activation of Nrf2 ( P <0. 01 , P <0. 05) in the reporter gene assay. As compared with control, three hepatotoxins ( APAP, CCl4 , Ethanol ) all decreased cell viability ( P<0. 01 ) , and baicalein significantly reversed such decreases in a concentra-tion-dependent manner ( P<0. 01 ) . Conclusion Ba-icalein can induce the activation of transcription factor Nrf2 , which is probably one of the mechanisms con-tributing to the protection of baicalein against hepato-toxins (APAP, CCl4, Ethanol)-induced hepatotoxici-ty.