About: The α7 nicotinic acetylcholine receptor agonist, GTS-21, attenuates hyperoxia-induced acute inflammatory lung injury by alleviating the accumulation of HMGB1 in the airways and the circulation

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About: The α7 nicotinic acetylcholine receptor agonist, GTS-21, attenuates hyperoxia-induced acute inflammatory lung injury by alleviating the accumulation of HMGB1 in the airways and the circulation Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	The α7 nicotinic acetylcholine receptor agonist, GTS-21, attenuates hyperoxia-induced acute inflammatory lung injury by alleviating the accumulation of HMGB1 in the airways and the circulation
Creator	Patel, Vivek Martino, Ashley Tracey, Kevin Ashby, Charles Gauthier, Alex Lin, Mosi Mantell, Lin Pavlov, Valentin Perron, Jeanette Sitapara, Ravikumar Valdés-Ferrer, Sergio Wang, Mao
Source	Medline; PMC
abstract	BACKGROUND: Oxygen therapy, using supraphysiological concentrations of oxygen (hyperoxia), is routinely administered to patients who require respiratory support including mechanical ventilation (MV). However, prolonged exposure to hyperoxia results in acute lung injury (ALI) and accumulation of high mobility group box 1 (HMGB1) in the airways. We previously showed that airway HMGB1 mediates hyperoxia-induced lung injury in a mouse model of ALI. Cholinergic signaling through the α7 nicotinic acetylcholine receptor (α7nAChR) attenuates several inflammatory conditions. The aim of this study was to determine whether 3–(2,4 dimethoxy-benzylidene)-anabaseine dihydrochloride, GTS-21, an α7nAChR partial agonist, inhibits hyperoxia-induced HMGB1 accumulation in the airways and circulation, and consequently attenuates inflammatory lung injury. METHODS: Mice were exposed to hyperoxia (≥99% O(2)) for 3 days and treated concurrently with GTS-21 (0.04, 0.4 and 4 mg/kg, i.p.) or the control vehicle, saline. RESULTS: The systemic administration of GTS-21 (4 mg/kg) significantly decreased levels of HMGB1 in the airways and the serum. Moreover, GTS-21 (4 mg/kg) significantly reduced hyperoxia-induced acute inflammatory lung injury, as indicated by the decreased total protein content in the airways, reduced infiltration of inflammatory monocytes/macrophages and neutrophils into the lung tissue and airways, and improved lung injury histopathology. CONCLUSIONS: Our results indicate that GTS-21 can attenuate hyperoxia-induced ALI by inhibiting extracellular HMGB1-mediated inflammatory responses. This suggests that the α7nAChR represents a potential pharmacological target for the treatment regimen of oxidative inflammatory lung injury in patients receiving oxygen therapy.
has issue date	2020-06-29(xsd:dateTime)
bibo:doi	10.1186/s10020-020-00177-z
bibo:pmid	32600307
has license	cc-by
sha1sum (hex)	8db6f35b6ac1c6eb31f965a9f06a91801f74ef45
schema:url	https://doi.org/10.1186/s10020-020-00177-z
resource representing a document's title	The α7 nicotinic acetylcholine receptor agonist, GTS-21, attenuates hyperoxia-induced acute inflammatory lung injury by alleviating the accumulation of HMGB1 in the airways and the circulation
has PubMed Central identifier	PMC7322715
has PubMed identifier	32600307
schema:publication	Mol Med
resource representing a document's body	covid:8db6f35b6ac1c6eb31f965a9f06a91801f74ef45#body_text
is schema:about of	named entity 'airways' named entity 'macrophages' named entity 'airways' named entity 'lung injury' named entity 'concentrations' named entity 'lung' named entity 'airways' named entity 'MG%' named entity 'INDICATED' named entity 'CONTROL' named entity 'MACROPHAGES' named entity '0.4' named entity 'TREATED' named entity 'MOUSE MODEL' named entity 'DECREASED' named entity 'aim' named entity 'HMGB1' named entity 'neutrophils' named entity 'α7 nicotinic acetylcholine receptor' named entity 'mediates' named entity 'However' named entity 'The' named entity 'determine' named entity 'levels' named entity 'attenuates' named entity 'ALI' named entity 'HMGB1' named entity 'anabaseine' named entity 'mouse model' named entity 'hyperoxia' named entity 'lung injury' named entity 'high mobility group' named entity 'histopathology' named entity 'hyperoxia' named entity 'ALI' named entity 'serum' named entity 'ALI' named entity 'hyperoxia' named entity 'HMGB1' named entity 'α7 nicotinic acetylcholine receptor' named entity 'HMGB1' named entity 'mice' named entity 'hyperoxia' named entity 'hematoxylin' named entity 'macrophages' named entity 'mice' named entity 'CD11c' named entity 'Extracellular' named entity 'intraperitoneal injection' named entity 'mouse models' named entity 'CD11b' named entity 'proinflammatory cytokine' named entity 'cellularization' named entity 'agonist' named entity 'horseradish peroxidase' named entity 'oxygen therapy' named entity 'preterm' named entity 'MCP-1' named entity 'alveolar' named entity 'caudally' named entity 'GTS-21' named entity 'ROS' named entity 'mice' named entity 'normal saline' named entity 'hyperoxia' named entity 'hyperoxia' named entity 'CD11b' named entity 'mice' named entity 'room temperature' named entity 'efferent'

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