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Abstract The objective of this study was to examine whether ultrasound can examine the development of cerebral vascular structure and cerebral blood flow in Sprague–Dawley (SD) rats by ultrasound in a noninvasive manner, which provides a reference for ultrasound research of SD rats. Thirty‐nine SD rats (7–16 days old) were divided into seven groups according to age, and the number of SD rats in each group was, respectively, 7, 17, 1, 3, 2, 8, and 1. Ultrasound was used to detect cerebral blood vessels, cerebrovascular flow velocity, and heart rate in SD rats in the sagittal and coronal positions, and images were obtained in B‐mode ultrasound. The cerebral vascular structure of 39 SD rats (7–16 days) was dynamically observed under B‐ultrasound. We found that the cerebral vascular structure of the rats aged 7–10 days was clear and detectable. Rats aged 11–16 days of cerebral vascular structures became thinner and undetectable. Quantitative analysis of cerebrovascular flow rate and heart rate in rats found that there was no significant difference in cerebrovascular blood flow rate and heart rate between 7 and 8 days. Ultrasound can also be used in rat animal studies, that is, the cerebral blood flow in rats of different ages can be monitored in real‐time by ultrasound in a noninvasive way.

Abstract The objective of the study is to investigate the brain development and atrophy of Diannan small‐ear pigs in different ages using magnetic resonance imaging (MRI). A total of 12 Diannan small‐ear pigs were included and divided into the young group, adult group, and middle‐and‐old age (M&O) group according to their age. The brain structure of pigs was scanned using MRI, and the brain data obtained were statistically analyzed by signal conversion and image reconstruction. Compared with the young group, the signals of most brain structures in the adult group and M&O group were significantly decreased (p

Abstract Neonatal hypoxic‐ischemic encephalopathy (NHIE) causes devastating cerebral damage and neurological deficits that seldom have effective therapies. This study aimed to explore the mechanisms underlying the therapeutic efficacy of Scutellarin in NHIE. NHIE models were successfully established. Zea‐longa score and triphenyte‐trazoliumchloride (TTC) staining demonstrated that hypoxia and ischemia (HI) insult induced prominent neurological dysfunctions and brain infarction. Protein microarray was applied to detect the differentially expressed genes in the cortex, hippocampus, and lung tissues of HI rats, which revealed the downregulation of vascular endothelial growth factor (VEGF) in these tissues. Additionally, double immunostaining uncovered VEGF expression was localized in the neurons. Besides, VEGF was decreasingly expressed in oxygen‐glucose deprivation (OGD) neurons, which was intriguingly reversed by Scutellarin treatment. Moreover, VEGF silencing increased OGD‐induced neuronal apoptosis and attenuated neurite outgrowth, which was enhanced by Scutellarin administration. GeneMANIA predicted a close correlation of VEGF with caspase 3, caspase 7, and interleukin (IL)‐1β, and qRT‐PCR revealed that Scutellarin treatment depressed the expression levels of them elevated in OGD neurons, but the Scutellarin‐depressed levels of these factors were prominently increased after VEGF silencing. Our findings suggested that Scutellarin exerted neuroprotective effects in NHIE potentially through mediating VEGF‐targeted inactivation of caspase 3, caspase 7, and IL‐1β.

Abstract Glioma is one of the most common primary brain tumors, and mortality due to this disease is second only to cardiovascular and cerebrovascular diseases. In traditional surgery, it is difficult to eradicate glioma; often recurrence increases its malignant degree, leading to a large number of patients killed by this disease. It is one of the most important subjects to study its pathogenesis and explore effective treatment methods. Research on glioma mechanisms mainly focuses on the effect of DNA methylation in epigenetics. Although there are many studies on protein phosphorylation, there is no overall regulatory mechanism. Protein phosphorylation regulates a variety of cell functions, such as cell growth, division and differentiation, and apoptosis. As a consequence, protein phosphorylation plays a leading part in various activities of glioma, and can also be used as a target to regulate the development of glioma. This review is aimed at studying the effect of protein phosphorylation on glioma, understanding the pathological mechanism, and an in‐depth analysis of it. The following is a discussion on glioma growth, migration and invasion, resistance and death in phosphorylation, and the possibility of treating glioma by phosphorylation.

Abstract Alzheimer's disease (AD) is a degenerative brain disease with complex clinical manifestations and pathogeneses such as abnormal deposition of beta‐amyloid protein and inflammation caused by the excessive activation of microglia. CXC motif chemokine receptor type 4 (CXCR4) is a type of G protein‐coupled receptor that binds to CXC motif ligand 12 (CXCL12) to activate downstream signaling pathways, such as the Janus kinase/signal transducer and activator of transcription and the renin–angiotensin system (Ras)/RAF proto‐oncogene serine (Raf)/mitogen‐activated protein kinase/extracellular‐regulated protein kinase; most of these signaling pathways are involved in inflammatory responses. CXCR4 is highly expressed in the microglia and astrocytes; this might be one of the important causes of inflammation caused by microglia and astrocytes. In this review, we summarize the mechanism and therapeutics of AD, the structures of CXCR4 and the CXCL12 ligand, and the mechanisms of CXCR4/CXCL12 that are involved in the occurrence and development of AD. The possible treatment of AD through microglia and astrocytes is also discussed, with the aim of providing a new method for the treatment of AD.

Abstract This study aimed to explore the possible target and mechanism of the wheel treadmill (WTM) test for motor function recovery of spinal cord injury (SCI). Rats were divided into sham, control and WTM groups to establish an SCI mode. Rats in the WTM group were trained on the WTM test, and Basso–Beattie–Bresnahan (BBB) scores were determined. The samples were collected, and mRNA sequencing was conducted to determine the changes in gene expression. The coexpressed genes were screened to construct a protein–protein interaction (PPI), followed by the Kyoto Encyclopedia of Genes and Genomes pathway and Gene Ontology function enrichment analysis, and the differentially expressed genes (DEGs) volcano map and hub gene expression heat map were constructed using R language. The BBB scores in the control and WTM groups increased with time, with the WTM group scoring higher than the control group. The results of rat spinal cord tissue sequencing showed that a total of 1679 DEGs were screened in the sham and control groups; 928 DEGs and 731 overlapping genes were screened in the WTM and control groups. The key genes were identified by PPI analysis. One hundred and thirty‐three genes were found to be overlapping by combined analysis of spinal cord sequencing data and BBB scores of rats at Week 7. The top 10 DEGs from high to low were Tyrobp, Rac2, Cd68, C1qb, Aif1, Cd74, Spi1, Fcer1g, RT1‐DA, and Ccl4. The terms with the highest enrichment scores were microglia‐mediated positive regulation of cytotoxicity and major histocompatibility complex class II protein complexes. Treatment with the WTM test promotes recovery of motor function after SCI in rats by modulating intercellular communication and immune function.

Background Hypoxic‐ischemic encephalopathy (HIE) could induce exacerbated changes and unpredictable effects in brain cells, and the mechanism remains unclear. Methods HIE model was established in neonatal rats, Zea‐Longa score and TTC staining were used to observe the neurobehavior and brain infarct volume in rats subjected to cerebral hypoxia‐ischemia (HI). Primary cortical neurons were then cultured in vitro to establish an oxygen and glucose deprivation model. To determine the role of synaptosomal‐associated protein‐25 (SNAP25) in HIE, PC12 cells were cultured and effective siRNA fragments were screened, and SNAP25 was transfected into primary neurons. Then, quantitative real‐time polymerase chain reaction was used to detect the mRNA expression level and immunofluorescence staining was used to observe the morphological changes of neurons before and after the injury. Finally, the abundance values of SNAP25 and its associated genes were filtered using the NCBI and GeneMANIA, respectively. Results HI leads to a decrease in neuronal number and an increase in SNAP25 expression. Whereas, the interference of SNAP25 caused marked decrease in neuronal number and the length of neurite. Moreover, the expression levels of CREB and SYP were significantly decreased after interference of SNAP25. Conclusion SNAP25 exhibited several neuroprotective effects to neuronal protection in neonatal cerebral HI by regulating CREB and SYP.

Objective To explore the role of Neurotropfin‐3 (NT‐3) in hypoxic‐ischemic encephalopathy (HIE) and determine its relative molecular mechanism. Methods The expression of NT‐3 was determined by qRT‐PCR in the cortex after HIE and immunofluorescence staining was used to detect the distribution of NT‐3. Then, the NT‐3 siRNA was used to validate the effect of NT‐3 for the neuroprotection by the measurement of cell apoptosis after oxygen‐glucose deprivation (OGD). Lastly, the molecular network mechanism was studied by NT‐3 interference experiment combined with bioinformatics technology. Results The expression of NT‐3 was significantly upregulated after HIE, and NT‐3 was co‐localized in the neurons of the cortex. Furthermore, the inhibition of NT‐3 increased neuronal apoptosis after OGD and elicited the down‐regulation of BDNF and NGF. Conclusion NT‐3 is a vital neurotrophic factor that can maintain neonatal survival in cortical neurons, and the underlying mechanism is associated with BDNF and NGF regulation.