神经发生
齿状回
溴脱氧尿苷
活性氧
神经干细胞
标记法
海马体
神经退行性变
丙二醛
抗氧化剂
生物
细胞凋亡
化学
内科学
内分泌学
细胞生物学
干细胞
细胞生长
生物化学
医学
疾病
作者
Qing Zhang,Xuekun Li,Xu Cui,Pingping Zuo
标识
DOI:10.1179/016164105x25126
摘要
We studied the effects of the reactive oxygen species (ROS) on neural progenitor cell proliferation and survival in the dentate gyrus (DG).The adult mice were treated with D-galactose for 7 weeks to mimic natural aging in mice. The level of malondialdehyde (MDA) and the activities of antioxidant enzymes in the serum were detected. Neurodegeneration and neurogenesis in the hippocampus were explored using terminal deoxynucleotidyltransferase-mediated UTP nick-end labeling (TUNEL) to detect the dying cells and bromodeoxyuridine (BrdU) was used to label the newly born cells.After the treatment of D-galactose, the level of MDA increased and the activities of the antioxidant enzyme decreased in the serum. TUNEL-positive cells significantly increased in the DG, CA1 and CA3 subfields. The BrdU-labeled proliferating cells and surviving cells in the DG decreased significantly in number after D-galactose treatment.D-Galactose induced the impairment of neurogenesis in the DG, which is similar to natural aging in mice. ROS accumulation as a result of D-galactose may be related to the decrease of neurogenesis in the DG.
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