Background: Inflammatory response mediated by microglia plays a key role in cerebral ischemia-reperfusion injury. This study intends to probe the role of lncRNA SNHG4 in regulating the inflammatory response of the microglia during cerebral ischemia reperfusion.
Materials And Methods: Blood samples and cerebrospinal fluid samples were collected from acute cerebral infarction (ACI) patients and healthy controls.
Adipose-derived stromal cells (ADSCs) have excellent capacities for regeneration and tissue protection, while sevoflurane, as a requisite component of surgical procedures, has shown therapeutic benefit in animal models of sepsis. This study therefore determined if the combination of sevoflurane and ADSCs exerted additional protective effects against acute lung injury (ALI) induced by cecal ligation and puncture (CLP) in rats. The animals were randomized into five groups: (sham operation (group I), CLP followed by mechanical ventilation (group II), CLP plus sevoflurane at 0.
View Article and Find Full Text PDFAdipose-derived stromal cells (ADSCs) showed excellent capacity in regeneration and tissue protection. Low tidal volume ventilation (LVT) strategy demonstrates a therapeutic benefit on the treatment of acute lung injury/acute respiratory distress syndrome (ALI/ARDS). This study, therefore, aimed to undertaken determine whether the combined LVT and ADSCs treatment exerts additional protection against lipopolysaccharide (LPS)-induced ALI in rats.
View Article and Find Full Text PDFSepsis-associated encephalopathy (SAE) is related to cognitive sequelae in patients in the intensive care unit and can have serious impacts on quality of life after recovery. Although various pathogenic pathways are involved in SAE development, little is known concerning the global role of long non-coding RNAs (lncRNAs) in SAE. Herein, we employed transcriptome sequencing approaches to characterize the effects of lipopolysaccharide (LPS) on lncRNA expression patterns in brain tissue isolated from Sprague-Dawley rats with and without SAE.
View Article and Find Full Text PDFSeveral studies have reported that neonatal exposure to propofol may cause neurotoxicity in the hippocampus, involving long-term neurodevelopmental impairments. We aimed to detect real-time changes of miR-132 of neonatal rats exposed to propofol anesthesia and to characterize subsequent changes in learning and memory. Seven-day-old Sprague-Dawley rats were injected intraperitoneally with 40mg/kg propofol at 0, 120, and 240 min or with isotonic fat emulsion as controls.
View Article and Find Full Text PDFPropofol exerts neurotoxic effects on the developing mammalian brains, but the underlying molecular mechanism remains unclear. MicroRNAs (miRNAs) are a class of small noncoding RNAs that modulate gene expression at the post-transcriptional level. However, in specific types of neurocytes, the detailed functions of miRNAs were not entirely understood.
View Article and Find Full Text PDFBackground/aims: Acute lung injury (ALI) and its aggressive stage, acute respiratory distress syndrome (ARDS), are characterized by diffuse damage and increased permeability of the endothelial barrier, leading to alveolar infiltrates and interstitial edema. Enhancing endothelial integrity represents a novel therapeutic strategy for ALI/ARDS. Endothelial progenitor cells (EPCs) have been reported to participate in endothelial repair of ALI and also serve as a tool for gene therapy.
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