Abstract:To investigate the protective effect of highly oxygenated water on the brain tissue of acutely hypoxic mice, a total of 80 SPF female Kunming mice were randomly divided into a control group and a highly oxygenated water group. After 30 days of treatment, the mice were further divided into four groups of 10 mice each for subsequent analysis. Three groups were used to determine the survival time in the atmospheric hypoxia experiment, sodium nitrite poisoning experiment, and acute cerebral hypoxia experiment. Additionally, brain tissue samples from the remaining 20 mice were immediately removed following death as a result of atmospheric pressure hypoxia, to detect the levels of HIF-1α and VEGF, as well as to assess the protein expression and mRNA levels of HIF-1α, VEGF, and AMPK. The results showed that, compared to the control group, the highly oxygenated water group exhibited extended survival times by 6.79%, 28.02%, and 10.83% in the three hypoxia experiments, respectively. Furthermore, the HIF-1α (P<0.05) and VEGF (P<0.01) levels were significantly reduced, the protein expressions of HIF-1α and VEGF were downregulated (P<0.05), and the mRNA level of HIF-1α was significantly increased (P<0.01). These results suggest that the intake of highly oxygenated water can promote the rapid adaptation of cells and tissues to acute hypoxia by depleting HIF-1α levels, regulating its transcription, and exerting a multi-directional hypoxia tolerance effect. In summary, short-term consumption of highly oxygenated water shows a protective effect on the brain tissue of acutely hypoxic mice.