Objective To explore the role of hydrogen sulfide (H 2S ) in acute liver injury induced by crush-ing hind lim bs of rats. Methods The rats w ere random ly divided into the follow ing groups:control, crush-ing, H 2S donor sodium hydrosulfide (NaHS) + crushing, H 2S inhibitor propargylglycine (PAG ) + crush-ing group. The acute liver injury m odel w as established by crushing the hind lim bs of rats w ith standard w eight. R ats w ere sacrificed at 30 m in and 120 m in after the crush. The activities of serum aspartate am inotransferase (AST) and alanine am inotransferase (ALT) w ere m easured by colorim etric m ethod, and the content of H 2S in plasm a and the contents of m alondialdehyde (MDA), protein carbonyl, glutathione (GSH) in the liver and the activity of H 2S generating enzym e (cystathionine γ-lyase, CSE) w ere deter-m ined by chem ical m ethod. The expression of CSEm R N Ain liver w as detected by R T-PCR . Results For crush injury group, the levels of ASTand ALTin serum , MDAand protein carbonyl in liver in-creased. The levels of GSH, CSE, CSEm R N Ain liver and H 2S in serum decreased. The adm inistration of NaHS before lim bs crush could attenuate the changes of liver injury, but the pre-treatm ent w ith PAG could exacerbate the changes. Conclusion The decrease of H 2S production could involve in m ediating the acute liver injury induced by traum atic stress in rats.