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http://purl.uniprot.org/citations/33168786http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/33168786http://www.w3.org/2000/01/rdf-schema#comment"Inflammation is known to play an important role in early brain injury (EBI) after subarachnoid hemorrhage (SAH). T cell immunoglobulin and mucin domain-3 (Tim-3) has emerged as a critical regulator of adaptive and innate immune responses, and has been identified to play a vital role in certain inflammatory diseases; The present study explored the effect of Tim-3 on inflammatory responses and detailed mechanism in EBI following SAH. We investigated the effects of Tim-3 on SAH models established by endovascular puncture method in Sprague-Dawley rats. The present studies revealed that SAH induced a significant inflammatory response and significantly increased Tim-3 expression. Tim-3-AAV administration aggravated neurocyte apoptosis, brain edema, blood-brain barrier permeability, and neurological dysfunction; significantly inhibited Nrf2 expression; and increased HMGB1 expression and secretion of pro-inflammatory cytokines, such as tumor necrosis factor alpha, interleukin (IL)-1 beta, IL-17, and IL-18. However, Tim-3 siRNA or NK252 administration abolished the pro-inflammatory effects of Tim-3. Our results indicate a function for Tim-3 as a molecular player that links neuroinflammation and brain damage after SAH. We reveal that Tim-3 overexpression deteriorates neuroinflammatory and neurocyte apoptosis after subarachnoid hemorrhage through the Nrf2/HMGB1 signaling pathway in rats."xsd:string
http://purl.uniprot.org/citations/33168786http://purl.org/dc/terms/identifier"doi:10.18632/aging.103796"xsd:string
http://purl.uniprot.org/citations/33168786http://purl.uniprot.org/core/author"He X."xsd:string
http://purl.uniprot.org/citations/33168786http://purl.uniprot.org/core/author"Li Y."xsd:string
http://purl.uniprot.org/citations/33168786http://purl.uniprot.org/core/author"Li R."xsd:string
http://purl.uniprot.org/citations/33168786http://purl.uniprot.org/core/author"Li X."xsd:string
http://purl.uniprot.org/citations/33168786http://purl.uniprot.org/core/author"Guo S."xsd:string
http://purl.uniprot.org/citations/33168786http://purl.uniprot.org/core/author"Liu W."xsd:string
http://purl.uniprot.org/citations/33168786http://purl.uniprot.org/core/author"Zhang X."xsd:string
http://purl.uniprot.org/citations/33168786http://purl.uniprot.org/core/author"Wei B."xsd:string
http://purl.uniprot.org/citations/33168786http://purl.uniprot.org/core/author"Cheng W."xsd:string
http://purl.uniprot.org/citations/33168786http://purl.uniprot.org/core/author"Duan C."xsd:string
http://purl.uniprot.org/citations/33168786http://purl.uniprot.org/core/date"2020"xsd:gYear
http://purl.uniprot.org/citations/33168786http://purl.uniprot.org/core/name"Aging (Albany NY)"xsd:string
http://purl.uniprot.org/citations/33168786http://purl.uniprot.org/core/pages"21161-21185"xsd:string
http://purl.uniprot.org/citations/33168786http://purl.uniprot.org/core/title"Tim-3 deteriorates neuroinflammatory and neurocyte apoptosis after subarachnoid hemorrhage through the Nrf2/HMGB1 signaling pathway in rats."xsd:string
http://purl.uniprot.org/citations/33168786http://purl.uniprot.org/core/volume"12"xsd:string
http://purl.uniprot.org/citations/33168786http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/33168786
http://purl.uniprot.org/citations/33168786http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/33168786
http://purl.uniprot.org/uniprot/#_P0C0K5-mappedCitation-33168786http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/33168786
http://purl.uniprot.org/uniprot/P0C0K5http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/33168786