Abstract
Neurogenesis is a physiological response after cerebral ischemic injury to possibly repair the damaged neural network. Therefore, promoting neurogenesis is very important for functional recovery after cerebral ischemic injury. Our previous research indicated that hyperbaric oxygen therapy (HBOT) exerted neuroprotective effects, such as reducing cerebral infarction volume. The purposes of this study were to further explore the effects of HBOT on the neurogenesis and the expressions of cell migration factors, including the stromal cell-derived factor 1 (SDF1) and its target receptor, the CXC chemokine receptor 4 (CXCR4). Thirty-two Sprague–Dawley rats were divided into the control or HBO group after receiving transient middle cerebral artery occlusion (MCAO). HBOT began to intervene 24 h after MCAO under the pressure of 3 atmospheres for one hour per day for 21 days. Rats in the control group were placed in the same acrylic box without HBOT during the experiment. After the final intervention, half of the rats in each group were cardio-perfused with ice-cold saline followed by 4% paraformaldehyde under anesthesia. The brains were removed, dehydrated and cut into serial 20μm coronal sections for immunofluorescence staining to detect the markers of newborn cell (BrdU+), mature neuron cell (NeuN+), SDF1, and CXCR4. The affected motor cortex of the other half rats in each group was separated under anesthesia and used to detect the expressions of brain-derived neurotrophic factor (BDNF), SDF1, and CXCR4. Motor function was tested by a ladder-climbing test before and after the experiment. HBOT significantly enhanced neurogenesis in the penumbra area and promoted the expressions of SDF1 and CXCR4. The numbers of BrdU+/SDF1+, BrdU+/CXCR4+, and BrdU+/NeuN+ cells and BDNF concentrations in the penumbra were all significantly increased in the HBO group when compared with the control group. The motor functions were improved in both groups, but there was a significant difference between groups in the post-test. Our results indicated that HBOT for 21 days enhanced neurogenesis and promoted cell migration toward the penumbra area in transient brain ischemic rats. HBOT also increased BDNF expression, which might further promote the reconstructions of the impaired neural networks and restore motor function.
Highlights
Stroke is a major cause of death and disability worldwide
The quantifications of BrdU+/CXC chemokine receptor 4 (CXCR4)+ cells (47.41 ± 3.18 cells) were significantly increased in the HBO group when compared with the control group (25.08 ± 4.34 cells, p < 0.01). These results indicated that hyperbaric oxygen therapy (HBOT) promoted the newborn cells migrating toward the penumbra area through the stromal cell-derived factor 1 (SDF1)-CXCR4 axis
The quantifications of BrdU+/NeuN+ cells (36.42 ± 3.08 cells) were significantly increased in the HBO group when compared with the control group (15.21 ± 5.86 cells, p < 0.01). These results indicated that the migratory progenitor cells were partially differentiated into the matured neurons and HBOT enhanced the differentiative properties
Summary
Stroke is a major cause of death and disability worldwide. Cerebral ischemic injury is the most common form of stroke. The field of the middle cerebral artery is the most common involved area in brain ischemic injury. The impaired areas of the brain after ischemic insult include the ischemic core and penumbra area [1]. The cells in the ischemic core area are necrotic and non-reversible. For the cells in the penumbra area, cell apoptosis is reduced if appropriate therapeutic interventions are given within a critical time limit. Early intervention to reduce cerebral ischemic injury has always been an important guideline for the clinical treatment of stroke patients
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