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胚胎期急性严重低氧常导致出生后运动失调、认知功能障碍和精神发育异常,目前仍缺乏有效的预防治疗手段。本研究旨在探讨以世代为单位的中海拔低氧环境适应是否对胚胎期急性严重低氧处理的小鼠有保护效应。以在昆明(海拔约1 900 m)饲养繁殖一年半,传代6~7代的ICR小鼠为研究对象,在妊娠9天(gestation day 9,GD 9)、13天(GD 13)或17天(GD 17)对孕鼠施加急性低氧处理(7%O_2,6 h),测试仔鼠出生后的发育情况、运动(旷场)、空间学习记忆(水迷宫)和焦虑水平(高架十字迷宫),并对相关脑区进行细胞计数。此外,还检测了生活在中海拔和低海拔地区小鼠的血液学指标。结果显示:(1)中海拔低氧环境适应良好的小鼠,其血液中的红细胞计数(red blood corpuscle count,RBC)、血红蛋白浓度(hemoglobin concentration,HBC)、红细胞压积(hematocrit,HCT)水平显著高于低海拔地区同性别的小鼠;(2)低氧组仔鼠的空间学习记忆能力没有损伤,并且GD 17组雌性仔鼠的空间记忆提取能力强于对照组;(3)低氧各组仔鼠均未见外观畸形和运动能力受损;(4)胚胎期低氧未造成仔鼠伏隔核、杏仁核和海马神经元发生明显坏死。以上结果提示中海拔低氧环境适应良好的小鼠遭遇胚胎期急性严重低氧时,其发育、运动和认知功能障碍程度明显轻于低海拔地区小鼠的,其保护机制可能是:经过数代中海拔低氧环境适应,ICR小鼠血液中的HBC和HCT增加。本研究的这些新发现可能会为探讨急性胚胎期低氧损伤作用和干预疗法提供依据。
Acute severe hypoxia in the embryo often leads to postnatal ataxia, cognitive dysfunction and mental retardation, and there is still no effective preventive treatment. This study aimed to investigate whether generational adaptation of mid-altitude hypoxia environment has protective effects on acute hypoxia-treated mice in embryonic stage. The ICR mice of six to seven generations were bred in Kunming (about 1 900 m above sea level) for one year and a half, and were treated with gestation day 9 (GD 9), 13 days (GD 13) or 17 Acute hypoxia (7% O_2, 6 h) was administered to pregnant rats to test the development, movement (open field), spatial learning and memory (maze) and anxiety levels of the offspring rats (GD 17) Maze), and the relevant brain area for cell counting. In addition, hematological markers were also tested in mice at mid-altitude and low altitudes. The results showed that: (1) red blood corpuscle count (RBC), hemoglobin concentration (HBC) and hematocrit (HCT) levels in blood of well-adapted mice in mid- (2) The spatial learning and memory abilities of pups in hypoxia group were not damaged, and the memory ability of female pups in GD 17 group was stronger than that of control group. (3) The hypoxia There was no appearance deformity and impaired motor ability in each group of pups. (4) The embryonic hypoxia did not cause obvious necrosis of nucleus accumbens, amygdala and hippocampus. The above results suggest that the well-adapted mice in mid-altitude hypoxia may experience developmental, motor and cognitive impairment when they are exposed to acute severe hypoxia in embryonic stage. The protective mechanism may be: In mid-low altitude hypoxia adaptation, ICH mice have increased HBC and HCT in their blood. These new findings in this study may provide the basis for exploring the role of hypoxic injury in acute embryonic stage and intervention therapy.