About: Phillyrin Relieves Lipopolysaccharide-Induced AKI by Protecting Against Glycocalyx Damage and Inhibiting Inflammatory Responses

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About: Phillyrin Relieves Lipopolysaccharide-Induced AKI by Protecting Against Glycocalyx Damage and Inhibiting Inflammatory Responses Goto Sponge NotDistinct Permalink

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

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Phillyrin Relieves Lipopolysaccharide-Induced AKI by Protecting Against Glycocalyx Damage and Inhibiting Inflammatory Responses
Creator	Zhang, Dong Huang, Xiao Wang, Xiaozhi Feng, Jiali Huang, Lina Li, Dongxiao Liu, Xiangyong Ma, Xiaohong Qi, Boyang
Source	PMC
abstract	Damage to the integrity of heparin sulfate (HS) in the endothelial glycocalyx is an important factor of glomerular filtration barrier dysfunction, which is the basic pathological feature of acute kidney injury (AKI). AKI is a common clinical critical illness with few drugs options offering effective treatment. Phillyrin (Phil), the main pharmacological component of Forsythia suspensa, possesses a wide range of pharmacological activities. However, the effects of Phil on lipopolysaccharide (LPS)-induced AKI have yet to be reported. The aim of the present study is to analyze the effects of Phil on HS damage and inflammatory signaling pathways in LPS-induced AKI. Results revealed that Phil reduces pathological changes and improves renal function in LPS-induced AKI. Further analysis indicated that Phil effectively protects against glycocalyx HS degradation in LPS-stimulated EA.hy926 cells in vitro and LPS-induced AKI mice in vivo. The protective effect of Phil on HS damage may be associated with the isolate’s ability to suppress the production of reactive oxygen species, and decrease expression levels of cathepsin L and heparanase in vitro and in vivo. In addition, ELISA and Western blot results revealed that Phil inhibits the activation of the NF-κB and MAPK signaling pathways and decreases the levels of inflammatory cytokines (IL-1β, IL-6, and TNF-α) in LPS-induced ARDS mice. In general, protection against endothelial glycocalyx HS damage and inhibition of inflammatory responses by Phil may be used as treatment targets for LPS-induced AKI.
has issue date	2019-12-12(xsd:dateTime)
bibo:doi	10.1007/s10753-019-01136-5
bibo:pmid	31832909
has license	no-cc
sha1sum (hex)	b15c9e62b023b8efceacb9522e9dbf80a7928789
schema:url	https://doi.org/10.1007/s10753-019-01136-5
resource representing a document's title	Phillyrin Relieves Lipopolysaccharide-Induced AKI by Protecting Against Glycocalyx Damage and Inhibiting Inflammatory Responses
has PubMed Central identifier	PMC7095384
has PubMed identifier	31832909
schema:publication	Inflammation
resource representing a document's body	covid:b15c9e62b023b8efceacb9522e9dbf80a7928789#body_text
is schema:about of	named entity 'lipopolysaccharide' named entity 'AKI' named entity 'barrier' named entity 'damage' named entity 'Inflammatory' named entity 'CRITICAL ILLNESS' named entity 'MAIN' named entity 'GENERAL' named entity 'PROTECTIVE EFFECT' named entity 'ADDITION' named entity 'EFFECTIVE' named entity 'COMPONENT' named entity 'HEPARIN SULFATE' named entity 'FORSYTHIA SUSPENSA' named entity 'NF-' named entity 'ability' named entity 'AKI' named entity 'ARDS' named entity 'AKI' named entity 'cytokines' named entity 'acute kidney injury' named entity 'inhibits' named entity 'Damage' named entity 'heparanase' named entity 'reactive oxygen species' named entity 'aim' named entity 'Responses' named entity 'reactive oxygen species' named entity 'mice' named entity 'renal function' named entity 'LPS' named entity 'LPS' named entity 'LPS' named entity 'glomerular filtration' named entity 'AKI' named entity 'glycocalyx' named entity 'mice' named entity 'AKI' named entity 'heparin sulfate' named entity 'LPS' named entity 'signaling pathways' named entity 'Phillyrin' named entity 'Lipopolysaccharide' named entity 'LPS' named entity 'protein' named entity 'IL-1β' named entity 'Serum' named entity 'room temperature' named entity 'LPS' named entity 'AKI' named entity 'glycocalyx' named entity 'NF-κB' named entity 'inflammatory response' named entity 'blood vessel' named entity 'TNF-α' named entity 'Triton X-100' named entity 'Santa Cruz Biotechnology' named entity 'extracellular' named entity 'expression levels' named entity 'glycocalyx' named entity 'Acute kidney injury' named entity 'ng/mL' named entity 'IκBα' named entity 'inflammatory responses' named entity 'nuclear transfer' named entity 'ROS' named entity 'Enzyme' named entity 'inflammatory reactions' named entity 'pathogenesis' named entity 'DAPI' named entity 'Shandong' named entity 'glycocalyx' named entity 'IL-1β'

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