ObjectiveTo explore the difference of anesthesia recovery and postoperative conscious state between remimazolam toluenesulfonic acid and propofol after induction and maintenance of general anesthesia.Methods104 patients undergoing elective tracheal intubation general anesthesia in our hospital were randomly divided into 2 groups: Remimazolam Toluenesulfonic acid group (Group R) and Propofol group (Group P). MOAA/S score, the modified Aldrete score, recovery index, time point, a state of consciousness, interpretative vital signs and adverse events were monitored at different time.ResultsCompared with the Group P, the extubation time and orientation recovery time of the Group R were significantly shorter. When the operation time was less than 1 hour, the MOAA/S score of the Group R was shorter than that of Group P at 5 min and 15 min after the operation. To compare with the Group P, the score of MOAA/S in the Group R increased at 5 min, 20 min and 30 min after the operation. When the operation time was less than or equal to 1 h, the modified Aldrete score in the Group R was slightly higher than that in the Group P at 30 min after extubation. There was no injection pain in the the Group R, and the incidence of hypotension was lower than that of propofol.ConclusionCompared with Propofol, when the operation time of general anesthesia is more than 1 hour, recovery time of Remimazolam Toluenesulfonic acid is shorter, with more complete and higher‐quality recovery.
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.
Background: Hypoxic-ischemic encephalopathy (HIE) could induce exacerbated changes and unpredictable efects 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 efective 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 iltered 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 signiicantly decreased after interference of SNAP25. Conclusion:SNAP25 exhibited several neuroprotective efects to neuronal protection in neonatal cerebral HI by regulating CREB and SYP. others promote neuronal death (Papadopoulos MC, et al., 2000). In addition, HIE is often difficult to diagnose in real time because of convulsions and other non-speciic encephalopathy, and is the most common reason of perinatal asphyxia (Zhang Y, et al., 2016). HIE can also lead to severe brain damage and is a common cause of neurological handicaps in adulthood (Kojima T, et al., 2013). Currently, there is no efective clinical treatments to mitigate HI-induced brain injury, due to the lack of understanding of the neural networks associated with HIinduced neurodegeneration and its mechanisms (Liu S, Article history:
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 immunoluorescence staining was used to detect the distribution of NT-3. Then, the NT-3 siRNA was used to validate the efect 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 signiicantly 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.
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,
Interleukin 10 (IL-10) is a synthetic inhibitor of human cytokines with immunomodulatory and anti-inflammatory effects. This study was designed to investigate the expression variation of IL-10 in the multiple sites including cortex, hippocampus, and lung tissues of neonatal hypoxic-ischemic (HI) rats and explore the crucial role of IL-10 in alleviating HI brain damage. In this study, neonatal Sprague-Dawley rats were subjected to the right common carotid artery ligation, followed by 2 h of hypoxia. The expression of IL-10 in the cortex, hippocampus, and lung tissues was measured with immunohistochemistry, real-time quantitative polymerase chain reaction (RT-qPCR), and western blot (WB). Immunofluorescence double staining was performed to observe the localization of IL-10 in neurons and astrocytes. Moreover, not-targeting and targeting IL-10 siRNA lentivirus vectors were injected into the rats of the negative control (NC) and IL-10 group, respectively, and the mRNA levels of B-cell lymphoma 2 (Bcl-2) and endoplasmic reticulum protein 29 (ERp29) were detected by RT-qPCR following IL-10 silence. The results demonstrated that the IL-10 expression was markedly increased after HI and IL-10 were colocalized with neurons and astrocytes which were badly injured by HI insult. In addition, Bcl-2 and ERp29 were remarkably decreased following IL-10 mRNA interference compared with the NC group. Our findings revealed that IL-10 exerted its antiapoptotic and neuroprotective effects by regulating the expression of Bcl-2 and ERp29, indicating that IL-10 may be a promising molecule target for HIE treatment.
ObjectiveThis study aimed to investigate the feasibility of Transcranial Doppler Ultrasonography (TCD) in evaluating neonatal hypoxic-ischemic encephalopathy (NHIE) modeling through monitoring the alteration of cerebrovascular flow in neonatal hypoxic-ischemic (HI) rats.MethodsPostnatal 7-day-old Sprague Dawley (SD) rats were divided into the control group, HI group, and hypoxia (H) group. TCD was applied to assess the changes of cerebral blood vessels, cerebrovascular flow velocity, and heart rate (HR) in sagittal and coronal sections at 1, 2, 3, and 7 days after the operation. For accuracy, cerebral infarct of rats was examined by 2,3,5-Triphenyl tetrazolium chloride (TTC) staining and Nissl staining to simultaneously verify the establishment of NHIE modeling.ResultsCoronal and sagittal TCD scans revealed obvious alteration of cerebrovascular flow in main cerebral vessels. Obvious cerebrovascular back-flow was observed in anterior cerebral artery (ACA), basilar artery (BA), middle cerebral artery (MCA) of HI rats, along with accelerated cerebrovascular flows in the left internal carotid artery (ICA-L) and BA, decreased flows in right internal carotid artery (ICA-R) relative to those in the H and control groups. The alterations of cerebral blood flows in neonatal HI rats indicated successful ligation of right common carotid artery. Besides, TTC staining further validated the cerebral infarct was indeed caused due to ligation-induced insufficient blood supply. Damage to nervous tissues was also revealed by Nissl staining.ConclusionCerebral blood flow assessment by TCD in neonatal HI rats contributed to cerebrovascular abnormalities observed in a real-time and non-invasive way. The present study elicits the potentials to utilize TCD as an effective means for monitoring the progression of injury as well as NHIE modeling. The abnormal appearance of cerebral blood flow is also beneficial to the early warning and effective detection in clinical practice.
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