Background: Ischemic tolerance is an endogenous protective mechanism in organs or tissues undergoing one or more short-term sublethal ischemias. Intermittent hypobaric hypoxia preconditioning (IHHP) can induce tolerance and thus protect brain tissues from cerebral ischemic injury (CIR). The current study evaluated the neuroprotective effect of IHHP.
Methods: The established xenograft model was divided into the ischemia/reperfusion (I/R), IHHP, IHHP+I/R, and sham groups. Transmission electron microscopy was used to observe alterations in neuron ultrastructure. Neuron damage was detected using Nissl staining. Western blot and qRT-PCR were used to evaluate the relative expression of genes and proteins related to apoptosis. Immunohistochemistry was used to determine the expression of proteins involved in the processes of neuroprotection and repair.
Results: Our results indicated that the damage to the neurons, organelles, and axons was significantly less following ischemia/reperfusion and intermittent hypobaric hypoxia reconditioning treatment than that in the ischemia/reperfusion group. Compared to the ischemia/reperfusion group, significant downregulation of pro-apoptotic gene/protein expressions along with upregulation of anti-apoptotic and nerve regeneration gene/protein expressions in the IHHP+I/R group were observed.
Conclusion: IHHP can significantly reduce ischemia/reperfusion injury in rat brain nerves and promote nerve repair.
Keywords: Intermittent hypobaric hypoxia; cerebral ischemia/reperfusion; neuroprotective; rats.
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