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http://dx.doi.org/10.1055/s-0041-1736571 | DOI Listing |
Semin Thromb Hemost
March 2022
Department of Biology, Faculty of Sciences Ain Chock, Immunology and Biodiversity Laboratory, Hassan II University, Casablanca.
J Neuroinflammation
June 2020
Department of Nursing, Division of Basic Medical Sciences, Research Center for Chinese Herbal Medicine, and Graduate Institute of Health Industry Technology, Chang Gung University of Science and Technology, 261 Wenhua 1st Road, Guishan, Taoyuan, Taiwan.
Background: Upregulation of matrix metalloproteinase-9 (MMP-9) has been indicated as one of the inflammatory biomarkers. In the central nervous system (CNS), the MMP-9 is induced by several proinflammatory mediators and participates in the CNS disorders, including inflammation and neurodegeneration. In addition, protein kinase Cs (PKCs) has been shown to be involved in regulation of various inflammatory factors like MMP-9 by several stimuli in many cell types.
View Article and Find Full Text PDFObjective: This study was performed to evaluate the regulating effects of acetylpuerarin on inflammation in an Alzheimer's disease (AD) rat model and an inflammatory cell model.
Methods: Healthy female Wistar rats and mouse BV2 microglia cells were selected. AD rat models were established with the method of bilateral intrahippocampal amyloid-β(Aβ)1-42 injections and the inflammatory cell models were established using Aβ25-35-induced mouse BV2 microglia cells.
Int J Med Sci
June 2016
1. Department of Anesthesiology and Pain Medicine, Gyeongsang National University School of Medicine and Gyeongsang National University Hospital, Jinju-si, 52727, Republic of Korea ; 6. Institute of Health Sciences, Gyeongsang National University, Jinju, Republic of Korea.
Vasoconstriction mediated by the highly selective alpha-2 adrenoceptor agonist dexmedetomidine leads to transiently increased blood pressure and severe hypertension. The dexmedetomidine-induced contraction involves the protein kinase C (PKC)-mediated pathway. However, the main PKC isoform involved in the dexmedetomidine-induced contraction remains unknown.
View Article and Find Full Text PDFBiochem Pharmacol
May 2013
Department of Emergency and Intensive Care Unit & Institute of Neuroscience, The First Affiliated Hospital of Soochow University, Suzhou 215006, PR China.
A-type K(+) channels are crucial in controlling neuronal excitability, and their regulation in sensory neurons may alter pain sensation. In this study, we identified the functional role of cobrotoxin, the short-chain α-neurotoxin isolated from Naja atra venom, which acts in the regulation of the transient A-type K(+) currents (IA) and membrane excitability in dorsal root ganglion (DRG) neurons via the activation of the muscarinic M3 receptor (M3R). Our results showed that cobrotoxin increased IA in a concentration-dependent manner, whereas the sustained delayed rectifier K(+) currents (IDR) were not affected.
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