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.
Highlights
It has been demonstrated that a sublethal ischemic/hypoxic exposure can improve the tolerance of tissue and/or cells to a subsequent lethal ischemic/hypoxic insult
We propose that expression of some hypoxia-inducible factor (HIF)-1 target genes, such as EPO and vascular endothelial growth factor (VEGF), may reach a high level induced by CoCl2 pretreatment and are no longer induced by hypoxia
The present study showed that CoCl2 pre-treatment increases hypoxic tolerance time, the abolishment time of Population Spikes (PS), HIF-1α level, HIF-1 target genes EPO and VEGF in a sort of plateau that is no longer inducible by hypoxia and repeated acute hypoxic stimuli
Summary
It has been demonstrated that a sublethal ischemic/hypoxic exposure can improve the tolerance of tissue and/or cells to a subsequent lethal ischemic/hypoxic insult This phenomenon is called ischemic/hypoxic preconditioning (I/HPC) and was first observed in the dog heart and later in the gerbil brain [1,2]. The salient aspect of this animal model is that the tolerance to hypoxia is increased with each exposure, and functions in an essentially linear arithmetic progression [7]. Using this model we have observed changes in molecules of the brain, including hypoxia-inducible factor (HIF)-1α, in developing hypoxic preconditioning in autoprogressive hypoxia [7,8,9]. We propose that HIF-1α can play an important role in contributing to neuron protection [7]
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