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目的研究高浓度氧(高氧)吸入对发育期小鼠脑的影响,探讨高氧暴露后脑细胞凋亡和内源性神经干细胞增殖的变化。方法将出生7d的C57/BL6小鼠置于高氧(75%)箱中5d,然后取出在正常环境中,腹腔注射5-溴脱氧尿核苷(BrdU),1次/d,连续5d。以同龄同室的小鼠作为空气对照组。用TUNEL方法检测脑组织凋亡细胞,免疫荧光法标记BrdU阳性的增殖细胞。结果高氧暴露组脑细胞凋亡数目(240.0±25.8)明显增多,与空气对照组(182.1±17.0)比较差异有统计学意义(t=8.677,P<0.001)。高氧暴露组海马齿状回颗粒下层的新生细胞数目(59.2±10.7)较对照组(49.3±8.7)明显增多,差异有统计学意义(t=3.998,P<0.001)。结论非生理性高氧暴露可介导发育期小鼠脑损伤,引起细胞调亡,并诱导脑内神经生发区的细胞增殖。
Objective To study the effect of high concentration oxygen (hyperoxia) inhalation on brain development in developing mice and to explore the changes of brain cell apoptosis and proliferation of endogenous neural stem cells after hyperoxia exposure. Methods C57 / BL6 mice 7d after birth were placed in hyperoxia (75%) for 5 days and then taken out. Normal environment, intraperitoneal injection of BrdU was given once a day for 5 days. The same age in the same room as the air control group mice. Apoptotic cells were detected by TUNEL method and BrdU positive proliferating cells were labeled by immunofluorescence. Results The number of apoptotic cells in the group exposed to hyperoxia increased significantly (240.0 ± 25.8), which was significantly different from that in the air group (182.1 ± 17.0) (t = 8.677, P <0.001). The number of newborn cells in inferior granular layer of hippocampal dentate gyrus in hypoxic exposure group (59.2 ± 10.7) was significantly higher than that in control group (49.3 ± 8.7), the difference was statistically significant (t = 3.998, P <0.001). Conclusion Non-physiological hyperoxia exposure can induce brain injury in mice during development, cause apoptosis and induce cell proliferation in neurobehavioral lesions in the brain.