The major neurodegenerative diseases are characterized by increasing of activated-microglial cells and inflammatory cytokines in the central nervous system. Carrageenan extracted from red algae is a kind of polysaccharide with sulfate groups. The oligosaccharides were obtained from carrageenan by enzymatic degradation. To detect the immunomodulatory activity of κ-carrageenan oligosaccharides (KOS) on microglial cells and the relationship to the sulfate group content, the desulfated derivatives of KOS (DSK) were obtained by dimethyl sulfoxide-methanol-pyridine method. KOS was labeled with fluorescein isothiocyanate. The effect of KOS and DSK on lipopolysaccharide (LPS)-activated microglial cells was detected. Hematoxylin-eosin staining and flow cytometric were used to detect the cell viability. The "scratch" migration assay, ornithine analysis and RT-PCR were used to determine the cell migration, arginase and TNF-α released by microglial cells, respectively. The effect of LPS and KOS on microglial cells was determined by flow cytometry and laser scanning confocal microscopy. The results showed that KOS and DSK could inhibit the cell viability, arginase and TNF-α released by LPS-activated microglia cell with concentration dependent manner. But the effect of DSK was weaker than that of KOS. KOS aggregated on the cell surface firstly, and then they enter into the cell to the nucleus, spread over the entire cell finally. But the exist of LPS could prevent the entrance of KOS. It could be concluded that KOS could protect microglial cells from being activated by LPS, and its inhibition function had relationship to the sulfate group content of KOS, while there were competition between LPS and KOS.
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http://dx.doi.org/10.1007/s11064-013-1228-4 | DOI Listing |
Front Cell Neurosci
December 2024
Department of Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Milan, Italy.
Introduction: Abnormal intracellular accumulation of Tau aggregates is a hallmark of Alzheimer's disease (AD) and other Tauopathies, such as Frontotemporal dementia (FTD). Tau deposits primarily affect neurons, but evidence indicates that glial cells may also be affected and contribute distinctively to disease progression. Cells can respond to toxic insults by orchestrating global changes in posttranslational modifications of their proteome.
View Article and Find Full Text PDFFront Immunol
December 2024
Emergency Department, Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, Shandong, China.
Objective: Subarachnoid hemorrhage (SAH) and tumorigenesis share numerous biological complexities; nevertheless, the specific gene expression profiles and underlying mechanisms remain poorly understood. This study aims to identify differentially expressed genes (DEGs) that could serve as biomarkers for diagnosis and prognosis.
Methods: Gene expression datasets (GSE122063, GSE13353, GSE161870) were analyzed using machine learning algorithms and logistic regression to identify DEGs associated with both SAH and tumorigenesis.
J Clin Periodontol
December 2024
Department of Periodontics, Liaoning Provincial Key Laboratory of Oral Diseases, School and Hospital of Stomatology, China Medical University, Shenyang, China.
Aim: Porphyromonas gingivalis, a consensus periodontal pathogen, is thought to be involved in Alzheimer's disease (AD) progression, and P. gingivalis-derived outer membrane vesicles (PgOMVs) are a key toxic factor in inducing AD pathology. This study aimed to clarify the regulatory mechanism underlying the PgOMV-induced AD-like phenotype.
View Article and Find Full Text PDFFEBS J
December 2024
Department of Neuroinflammation, UCL Queen Square Institute of Neurology, University College London, UK.
The microglial triggering receptor expressed on myeloid cells 2 (TREM2) is required for diverse microglia responses in neurodegeneration, including immunometabolic plasticity, phagocytosis, and survival. We previously identified that patient iPSC-derived microglia (iPS-Mg) harboring the Alzheimer's disease (AD) TREM2 hypomorph display several functional deficits linked to metabolism. To investigate whether these deficits are associated with disruptions in metabolite signaling, we generated common variant, TREM2 and TREM2 variant human iPS-Mg.
View Article and Find Full Text PDFBrain Behav
December 2024
Department of Anesthesiology, The Third Hospital of Hebei Medical University, Shijiazhuang, China.
Purpose: This study aims to explore the neuroprotective effect of propofol in improving traumatic brain injury (TBI) by inhibiting ferroptosis through the modulation of the endothelial nitric oxide (NO) synthase (eNOS)/NO signaling pathway.
Methods: The GSE173975 dataset was used to analyze the differentially expressed genes between TBI and sham surgery control groups in the short and long term. A TBI model was established in 2-month-old male SPF C57BL/6 mice by impact exposure of the exposed dura mater.
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