Objective To detect the effect of profound hypothermia on Bax expression and its relationship with cell apoptosis in the rat hippocampus after global ischemia. Methods Animal models of cardiopulmonary bypass (CPB) were established in 30 Wistar rats which were randomized into blank control group (rats were sacrificed 5 min after model making and hippocampus tissues were prepared), normothermia ischemia group (circulatory arrest was performed at [37.0±0.3]°C for 5 min, and then, rats were sacrificed 5 min after model making and hippocampus tissues were prepared) and hypothermia ischemia group (circulatory arrest was performed at [18.0±0.5]°C by ice crumbles for 5 min, and then, rats were sacrificed 5 min after model making and hippocampus tissues were prepared, n=10). Quantitative real-time PCR (qPCR) was used to detect the Bax mRNA expression, immunohistochemical method was used to detect the Bax protein expression, Western blotting was used to detect the cytochrome C (Cyt-C) expression, and TUNEL was used to measure the cell apoptosis. Results The Bax mRNA expression (2.734±0.301), optical density of positive cells (0.326±0.017), Cyt-C protein expression (4.14 ±0.79) and cell apoptosis rate (53.95％±4.23％) increased significantly in the normothermia ischemia group as compared with those in the blank control group (P<0.05). The Bax mRNA expression (1.679 ±0.309), optical density of positive cells (0.209 ±0.019), Cyt-C protein expression (1.45±0.49) and cell apoptosis rate (15.56％±3.02％) in the hypothermia ischemia group decreased significantly as compared with those in the normothermia ischemia group (P<0.05).Conclusion By inhibiting the expression of Bax, profound hypothermia can inhibit release of Cyt-C into the cytoplasm and thus reduce cell apoptosis in the hippocampus after global ischemia in rats, which may be one important way that profound hypothermia has protective effect on brain tissue with ischemic injury.