OBJECTIVE: To observe the effect of gangliosides (GM1) on the apoptosis and expression of Bax and Bcl-2, two genes involved in apoptosis. METHODS: An HIE model was produced in 7day old SpragueDawley (SD) rats by unilateral carotid artery ligation followed by hypoxic insult (8% oxygen) for 2.5 hours. Six of these HIE rats were treated promptly with GM1 (30 mg/kg daily for 3 days) and 6 were not given any treatment as the controls. Apoptosis was examined using terminal deoxynucleotidyl transferase mediated dUTP biotin nick end labelling (TUNEL) staining and the expression of Bax and Bcl-2 was detected by the immunohistochemical streptoavidinbiotinperoxidase complex (SABC) method in all neonatal rats. RESULTS: Apoptosis was noted in the cerebral neurons of the neonatal rats after HI injuries. Apoptosis secondary to HI could be eliminated with prompt treatment with GM1 after the HI insult. The number of apoptotic cells in the cortex and hippocampus decreased from 75.25±4.94 and 47.25±6.6 to 55.75±6.71 and 32.14±4.88 respectively (P<0.01). Bax and Bcl-2 were expressed in all neonatal rats. Bax was expressed to a greater extent and Bcl-2 to a lesser extent in HIE neonatal rats compared with neonatal rats with prompt treatment with GM1(P<0.05). CONCLUSIONS: Prompt treatment with GM1 after HI injuries in neonatal rats results in decreased neuronal apoptosis. GM1 could partly affect the expression of Bax and Bcl-2. The results suggest that neonatal neuronal apoptosis after HI injuries may be related to changes in the expression of these two genes.