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在使用小鼠模型的自进展性缺氧实验条件下,氯化钴对缺氧诱导因子-1α蛋白的影响。

The effects of CoCl2 on HIF-1α protein under experimental conditions of autoprogressive hypoxia using mouse models.

作者信息

Zhang Yan-Bo, Wang Xiulian, Meister Edward A, Gong Ke-Rui, Yan Shao-Chun, Lu Guo-Wei, Ji Xun-Ming, Shao Guo

机构信息

Department of Neurology, Affiliated Hospital of Tai Shan Medical University, Taishan 271000, China.

Department of Intensive Care Unit , 2nd Affiliated Hospital of Baotou Medical College, Baotou 014030, China.

出版信息

Int J Mol Sci. 2014 Jun 18;15(6):10999-1012. doi: 10.3390/ijms150610999.

DOI:10.3390/ijms150610999
PMID:24945310
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4100194/
Abstract

It is well known that cobalt chloride (CoCl2) can enhance the stability of hypoxia-inducible factor (HIF)-1α. The aim of this study is to detect the effect of CoCl2 on the hypoxia tolerance of mice which were repeatedly exposed to autoprogressive hypoxia. Balb/c mice were randomly divided into groups of chemical pretreatment and normal saline (NS), respectively injected with CoCl2 and NS 3 h before exposure to hypoxia for 0 run (H0), 1 run (H1), and 4 runs (H4). Western Blot, electrophoretic mobility shift assay (EMSA), extracellular recordings population spikes in area cornus ammonis I (CA 1) of mouse hippocampal slices and real-time were used in this study. Our results demonstrated that the tolerance of mice to hypoxia, the changes of HIF-1α protein level and HIF-1 DNA binding activity in mice hippocampus, the mRNA level of erythropoietin (EPO) and vascular endothelial growth factor (VEGF), and the disappearance time of population spikes of hippocampal slices were substantially different between the control group and the CoCl2 group. Over-induction of HIF-1α by pretreatment with CoCl2 before hypoxia did not increase the hypoxia tolerance.

摘要

众所周知,氯化钴(CoCl2)可增强缺氧诱导因子(HIF)-1α的稳定性。本研究旨在检测CoCl2对反复暴露于自动渐进性缺氧的小鼠缺氧耐受性的影响。将Balb/c小鼠随机分为化学预处理组和生理盐水(NS)组,分别在缺氧暴露前3小时注射CoCl2和NS,进行0次(H0)、1次(H1)和4次(H4)缺氧暴露。本研究采用蛋白质免疫印迹法(Western Blot)、电泳迁移率变动分析(EMSA)、小鼠海马切片海马杏仁核I区(CA 1)细胞外记录群体峰电位以及实时定量PCR。我们的结果表明,对照组和CoCl2组小鼠的缺氧耐受性、小鼠海马中HIF-1α蛋白水平和HIF-1 DNA结合活性的变化、促红细胞生成素(EPO)和血管内皮生长因子(VEGF)的mRNA水平以及海马切片群体峰电位的消失时间存在显著差异。缺氧前用CoCl2预处理过度诱导HIF-1α并没有增加缺氧耐受性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2ce/4100194/e2984fb7b6db/ijms-15-10999-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2ce/4100194/c78b10584cb6/ijms-15-10999-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2ce/4100194/c52340650f5a/ijms-15-10999-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2ce/4100194/9a211f942250/ijms-15-10999-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2ce/4100194/dfc48af427a7/ijms-15-10999-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2ce/4100194/b72e1cf558c5/ijms-15-10999-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2ce/4100194/e2984fb7b6db/ijms-15-10999-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2ce/4100194/c78b10584cb6/ijms-15-10999-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2ce/4100194/c52340650f5a/ijms-15-10999-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2ce/4100194/9a211f942250/ijms-15-10999-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2ce/4100194/dfc48af427a7/ijms-15-10999-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2ce/4100194/b72e1cf558c5/ijms-15-10999-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2ce/4100194/e2984fb7b6db/ijms-15-10999-g006.jpg

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