Objective To observe the changes of nitric oxide ( NO) and hydrogen sulfide ( H2 S) levels in the liver tissue of rabbit with nonalcoholic fatty liver disease ( NAFLD ) ，and explore the effect of NOand H2 S in the pathogenesis of NAFLD. Methods Forty Japanese white rabbits were randomly divided into severe NAFLD group，mild NAFLD group，and blank control group. The severe NAFLD group was given high fat diet 160 g /rabbit. day，the mild NAFLD group was given high fat diet 80 g /rabbit. day and normal diet 80 g /rabbit. day，and the blank control group was given normal diet160 g /rabbit. day. The raising cycle was 13 weeks. Plasma samples were collected before and after the experiment，and the concentration of triglyceride ( TG) ，cholesterol ( TC) ，and the levels of NO and H2 S in the liver tissue were determined. Pathological changes of the liver tissue were examined by light microscopy with HEstaining. Results (1) TC and TG levels: There was no significant difference between the mild and blank control groups ( P > 0. 05) . After the high diet feeding，the TC and TG were ( 32. 12 ± 1. 25 ) and ( 6. 02 ± 2. 12 ) nmol /L in the severe NAFLD group，(18. 34 ± 2. 10) and (4. 39 ± 1. 93) nmol /L in the mild NAFLD group，respectively，before experiment ( P < 0. 01) ，and those in the severe were also significantly higher than thosein the mild NAFLD group (P < 0. 01) . (2) The NO level in the liver tissue: It was (132. 4 ± 20. 7)μmol / g. pro in the severe，(95. 4 ± 19. 8)μmol / g. pro in the mild NAFLD group，and (74. 9 ± 34. 7) μmol / g. pro in the blank control group，with a very significant difference between the severe and mild NAFLD groups，and between the two NAFLD and the blank control groups. (3) The H2S level in the liver tissue of the severe and mild NAFLD groups was significantly decreased，compared with that in the blank control group ( P < 0. 01) ，and between the severe and mild NAFLD groups ( P < 0. 05) . (4) Liver pathology: Moderate changes were seen in the severe NAFLD group，slight to moderate changes in the mild NAFLD group，and normal histological appearance in the liver tissue of the blank control group. Conclusions NO and H2S participate the pathogenesis of nonalcoholic fatty liver disease. It is possible that intervention of the NO and H2S may become another future direction in prevention of this disease.