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新生大鼠缺氧/缺血性脑损伤时皮层神经元HIF-1α的表达与凋亡相关基因P53、Bcl-2的关系
作者:王娟 张玉真 蒋犁 
单位:东南大学临床医学院
关键词: 缺氧诱导因子-1α 未成熟脑 缺氧缺血 凋亡 大脑皮质 
分类号:
出版年·卷·期(页码):2011·30·第二期(319-323)
摘要:

目的 探讨未成熟脑缺氧缺血性脑损伤时皮层神经元缺氧诱导因子-1α(HIF-1α)的表达及其与P53、Bcl-2的关系。方法 新生7日龄SD大鼠随机分为假手术(Sham)组、单纯缺氧(H)组和缺氧缺血(HI)组,在缺氧/缺氧缺血后3h、6h、12h、24h及72h断头取脑。HE染色观察脑组织病理改变,免疫组化方法检测皮层神经元HIF-1α、P53及Bcl-2表达情况。结果 HE染色显示H组和HI组大脑皮层神经元都有不同程度的损伤,于24h时损伤最重,细胞溶解缺失明显。H组和HI组皮层HIF-1α于缺氧/缺氧缺血后3h表达升高,12h达高峰,之后呈下降趋势。H组和HI组皮层P53表达高峰较HIF-1α推后,24h达高峰,之后呈下降趋势。H组和HI组Bcl-2表达规律与HIF-1α一致。Sham组P53/ Bcl-2比值约等于1,H组和HI组3h、6h和12h这三个时间点上P53/ Bcl-2比值小于1,H组和HI组24h和72h这两个时间点上P53/ Bcl-2比值大于1。结论 未成熟脑缺氧缺血性脑损伤时,HIF-1α参与了对P53及Bcl-2的调控,在缺氧损伤早期可能具有抗凋亡作用。

Objective To investigate the expression of HIF-1α and the relationship between HIF-1α and P53,Bcl-2 in immature brain after hypoxia ischemia brain damage. Methods Postnatal day 7 SD rats were divided into three groups: sham group, the hypoxia group and the hypoxia-ischemia group. Rats were collected at 3h, 6h, 12h, 24h and 72h after hypoxia or hypoxia ischemia from each group. HE staining was used to detect histopathological damage. Immunohistochemistry was used to detect the expression of HIF-1α, P53 and Bcl-2. Results HE staining showed that neuronal degeneration and edema became prominent at 24h after hypoxia and hypoxia ischemia. The expression of HIF-1α protein was significantly upregulated at 3h, peak at 12h, and then decreased after hypoxia and hypoxia ischemia in both hypoxia and hypoxia ischemia group. The expression of P53 protein was upregulated at 3h, peak at 24h, and then decreased after hypoxia and hypoxia ischemia in the two groups. The expression of Bcl-2 protein was similar with HIF-1α in both groups. The rate of P53 and Bcl-2 was almost 1 in sham group, less than 1 at 3h, 6h and 12h in both hypoxia and hypoxia ischemia groups, and more than 1 at 24h and 72h in both hypoxia and hypoxia ischemia groups. Conclusion The HIF-1α participates in the regulation of P53 and Bcl-2 in immature brain after hypoxia ischemia brain damage. HIF-1α may have protective role in the onset of hypoxia.

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