论文部分内容阅读
目的:观察1,6-二磷酸果糖对亚急性一氧化碳中毒(CO)致迟发性脑损伤的防护作用。方法:小鼠腹腔注射CO 100 mL/kg,每天一次,连续7天。停止给予CO后,观察小鼠死亡率,学习记忆能力改变,脑组织病理学和单胺氧化酶-B活性的改变;FDP在每次给予CO前30 min腹腔注射。结果:FDP预先给予CO中毒小鼠能显著降低死亡率,显著改善学习记忆能力;防止海马细胞延迟性死亡;并能阻遏单胺类氧化酶-B活性的升高。结论:1,6-二磷酸果糖预防性给药对亚急性一氧化碳中毒致迟发性脑损伤有明显的防护作用。
Objective: To observe the protective effect of fructose 1,6-diphosphate on delayed brain injury induced by subacute carbon monoxide poisoning (CO). METHODS: Mice were injected intraperitoneally with CO 100 mL / kg once daily for 7 days. After stopping the administration of CO, the mice were observed for mortality, changes in learning and memory ability, brain histopathology and activity of monoamine oxidase-B; FDP was injected intraperitoneally 30 min before each administration of CO. Results: FDP pretreatment CO poisoning mice can significantly reduce mortality, significantly improve learning and memory ability; prevent delayed death of hippocampal cells; and can inhibit the monoamine oxidase - B activity. CONCLUSION: Pretreatment with fructose-1,6-diphosphate has a significant protective effect on delayed brain injury induced by subacute carbon monoxide poisoning.