C-C motif chemokine ligand 2 (CCL2) is a member of the monocyte chemokine protein family, which binds to its receptor CCR2 to induce monocyte infiltration and mediate inflammation. The CCL2/CCR2 signaling pathway participates in the transduction of neuroinflammatory information between all types of cells in the central nervous system. Animal studies and clinical trials have shown that CCL2/CCR2 mediate the pathological process of ischemic stroke, and a higher CCL2 level in serum is associated with a higher risk of any form of stroke. In the acute phase of cerebral ischemia-reperfusion, the expression of CCL2/CCR2 is increased in the ischemic penumbra, which promotes neuroinflammation and enhances brain injury. In the later phase, it participates in the migration of neuroblasts to the ischemic area and promotes the recovery of neurological function. CCL2/CCR2 gene knockout or activity inhibition can reduce the nerve inflammation and brain injury induced by cerebral ischemia-reperfusion, suggesting that the development of drugs regulating the activity of the CCL2/CCR2 signaling pathway could be used to prevent and treat the cell injury in the acute phase and promote the recovery of neurological function in the chronic phase in ischemic stroke patients.

Nucleosomes composed of histone octamer and DNA are the basic structural unit in the eukaryote chromosome. Under the stimulation of various factors, histones will undergo posttranslational modifications such as methylation, phosphorylation, acetylation, and ubiquitination, which change the three-dimensional structure of chromosomes and affect gene expression. Therefore, the combination of different states of histone modifications modulates gene expression is called histone code. The formation of learning and memory is one of the most important mechanisms for animals to adapt to environmental changes. A large number of studies have shown that histone codes are involved in the formation and consolidation of learning and memory. Here, we review the most recent literature of histone modification in regulating neurogenesis, dendritic spine dynamic, synapse formation, and synaptic plasticity.

Among cerebrovascular diseases, ischemic stroke is a leading cause of mortality and disability. Thrombolytic therapy with tissue plasminogen activator is the first choice for clinical treatment, but its use is limited due to the high requirements of patient characteristics. Therefore, the choice of neurological rehabilitation strategies after stroke is an important prevention and treatment strategy to promote the recovery of neurological function in patients. This study shows that rehabilitation exercise 24 h after stroke can significantly improve the neurological function (6.47 ± 1.589 vs. 3.21 ± 1.069 and 0.76 ± 0.852), exercise ability (15.68 ± 5.95 vs. 162.32 ± 9.286 and 91.18 ± 7.377), daily living ability (23.37 ± 5.196 vs. 66.95 ± 4.707 and 6.55 ± 2.873), and quality of life (114.39 ± 7.772 vs. 168.61 ± 6.323 and 215.95 ± 10.977) of patients after 1 month and 3 months, and its ability to promote rehabilitation is better than that of rehabilitation exercise administered to patients 72 h after stroke (p < 0.001). Animal experiments show that treadmill exercise 24 h after middle cerebral artery occlusion and reperfusion can inhibit neuronal apoptosis, reduce the volume of cerebral infarction on the third (15.04 ± 1.07% vs. 30.67 ± 3.06%) and fifth (8.33 ± 1.53% vs. 30.67 ± 3.06%) days, and promote the recovery of neurological function on the third (7.22 ± 1.478 vs. 8.28 ± 1.018) and fifth (4.44 ± 0.784 vs. 6.00 ± 0.767) days. Mechanistic studies have shown that treadmill exercise increases the density of microvessels, regulates angiogenesis, and promotes the recovery of nerve function by upregulating the expression of vascular endothelial growth factor and laminin. This study shows that rehabilitation exercise 24 h after stroke is conducive to promoting the recovery of patients’ neurological function, and provides a scientific reference for the clinical rehabilitation of stroke patients.