PubMed:25361765
Annnotations
Inflammaging
{"project":"Inflammaging","denotations":[{"id":"T1","span":{"begin":0,"end":96},"obj":"Sentence"},{"id":"T2","span":{"begin":97,"end":314},"obj":"Sentence"},{"id":"T3","span":{"begin":315,"end":418},"obj":"Sentence"},{"id":"T4","span":{"begin":419,"end":552},"obj":"Sentence"},{"id":"T5","span":{"begin":553,"end":648},"obj":"Sentence"},{"id":"T6","span":{"begin":649,"end":811},"obj":"Sentence"},{"id":"T7","span":{"begin":812,"end":951},"obj":"Sentence"},{"id":"T8","span":{"begin":952,"end":1026},"obj":"Sentence"},{"id":"T9","span":{"begin":1027,"end":1167},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":96},"obj":"Sentence"},{"id":"T2","span":{"begin":97,"end":314},"obj":"Sentence"},{"id":"T3","span":{"begin":315,"end":418},"obj":"Sentence"},{"id":"T4","span":{"begin":419,"end":552},"obj":"Sentence"},{"id":"T5","span":{"begin":553,"end":648},"obj":"Sentence"},{"id":"T6","span":{"begin":649,"end":811},"obj":"Sentence"},{"id":"T7","span":{"begin":812,"end":951},"obj":"Sentence"},{"id":"T8","span":{"begin":952,"end":1026},"obj":"Sentence"},{"id":"T9","span":{"begin":1027,"end":1167},"obj":"Sentence"}],"text":"Soluble epoxide hydrolase as an anti-inflammatory target of the thrombolytic stroke drug SMTP-7.\nAlthough ischemic stroke is a major cause of death and disability worldwide, only a small fraction of patients benefit from the current thrombolytic therapy due to a risk of cerebral hemorrhage caused by inflammation. Thus, the development of a new strategy to combat inflammation during thrombolysis is an urgent demand. The small molecule thrombolytic SMTP-7 effectively treats ischemic stroke in several animal models with reducing cerebral hemorrhage. Here we revealed that SMTP-7 targeted soluble epoxide hydrolase (sEH) to suppress inflammation. SMTP-7 inhibited both of the two sEH enzyme activities: epoxide hydrolase (which inactivates anti-inflammatory epoxy-fatty acids) and lipid phosphate phosphatase. SMTP-7 suppressed epoxy-fatty acid hydrolysis in HepG2 cells in culture, implicating the sEH inhibition in the anti-inflammatory mechanism. The sEH inhibition by SMTP-7 was independent of its thrombolytic activity. The simultaneous targeting of thrombolysis and sEH by a single molecule is a promising strategy to revolutionize the current stroke therapy."}
sentences
{"project":"sentences","denotations":[{"id":"T1","span":{"begin":0,"end":96},"obj":"Sentence"},{"id":"T2","span":{"begin":97,"end":314},"obj":"Sentence"},{"id":"T3","span":{"begin":315,"end":418},"obj":"Sentence"},{"id":"T4","span":{"begin":419,"end":552},"obj":"Sentence"},{"id":"T5","span":{"begin":553,"end":648},"obj":"Sentence"},{"id":"T6","span":{"begin":649,"end":811},"obj":"Sentence"},{"id":"T7","span":{"begin":812,"end":951},"obj":"Sentence"},{"id":"T8","span":{"begin":952,"end":1026},"obj":"Sentence"},{"id":"T9","span":{"begin":1027,"end":1167},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Soluble epoxide hydrolase as an anti-inflammatory target of the thrombolytic stroke drug SMTP-7.\nAlthough ischemic stroke is a major cause of death and disability worldwide, only a small fraction of patients benefit from the current thrombolytic therapy due to a risk of cerebral hemorrhage caused by inflammation. Thus, the development of a new strategy to combat inflammation during thrombolysis is an urgent demand. The small molecule thrombolytic SMTP-7 effectively treats ischemic stroke in several animal models with reducing cerebral hemorrhage. Here we revealed that SMTP-7 targeted soluble epoxide hydrolase (sEH) to suppress inflammation. SMTP-7 inhibited both of the two sEH enzyme activities: epoxide hydrolase (which inactivates anti-inflammatory epoxy-fatty acids) and lipid phosphate phosphatase. SMTP-7 suppressed epoxy-fatty acid hydrolysis in HepG2 cells in culture, implicating the sEH inhibition in the anti-inflammatory mechanism. The sEH inhibition by SMTP-7 was independent of its thrombolytic activity. The simultaneous targeting of thrombolysis and sEH by a single molecule is a promising strategy to revolutionize the current stroke therapy."}
PubmedHPO
{"project":"PubmedHPO","denotations":[{"id":"T1","span":{"begin":106,"end":121},"obj":"HP_0002140"},{"id":"T2","span":{"begin":115,"end":121},"obj":"HP_0001297"},{"id":"T3","span":{"begin":271,"end":290},"obj":"HP_0001342"},{"id":"T4","span":{"begin":477,"end":492},"obj":"HP_0002140"},{"id":"T5","span":{"begin":486,"end":492},"obj":"HP_0001297"},{"id":"T6","span":{"begin":532,"end":551},"obj":"HP_0001342"},{"id":"T7","span":{"begin":1152,"end":1158},"obj":"HP_0001297"}],"text":"Soluble epoxide hydrolase as an anti-inflammatory target of the thrombolytic stroke drug SMTP-7.\nAlthough ischemic stroke is a major cause of death and disability worldwide, only a small fraction of patients benefit from the current thrombolytic therapy due to a risk of cerebral hemorrhage caused by inflammation. Thus, the development of a new strategy to combat inflammation during thrombolysis is an urgent demand. The small molecule thrombolytic SMTP-7 effectively treats ischemic stroke in several animal models with reducing cerebral hemorrhage. Here we revealed that SMTP-7 targeted soluble epoxide hydrolase (sEH) to suppress inflammation. SMTP-7 inhibited both of the two sEH enzyme activities: epoxide hydrolase (which inactivates anti-inflammatory epoxy-fatty acids) and lipid phosphate phosphatase. SMTP-7 suppressed epoxy-fatty acid hydrolysis in HepG2 cells in culture, implicating the sEH inhibition in the anti-inflammatory mechanism. The sEH inhibition by SMTP-7 was independent of its thrombolytic activity. The simultaneous targeting of thrombolysis and sEH by a single molecule is a promising strategy to revolutionize the current stroke therapy."}
mondo_disease
{"project":"mondo_disease","denotations":[{"id":"T1","span":{"begin":77,"end":83},"obj":"Disease"},{"id":"T3","span":{"begin":115,"end":121},"obj":"Disease"},{"id":"T5","span":{"begin":301,"end":313},"obj":"Disease"},{"id":"T6","span":{"begin":365,"end":377},"obj":"Disease"},{"id":"T7","span":{"begin":486,"end":492},"obj":"Disease"},{"id":"T9","span":{"begin":635,"end":647},"obj":"Disease"},{"id":"T10","span":{"begin":1152,"end":1158},"obj":"Disease"}],"attributes":[{"id":"A1","pred":"mondo_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/MONDO_0005098"},{"id":"A2","pred":"mondo_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/MONDO_0011057"},{"id":"A3","pred":"mondo_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/MONDO_0005098"},{"id":"A4","pred":"mondo_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/MONDO_0011057"},{"id":"A5","pred":"mondo_id","subj":"T5","obj":"http://purl.obolibrary.org/obo/MONDO_0021166"},{"id":"A6","pred":"mondo_id","subj":"T6","obj":"http://purl.obolibrary.org/obo/MONDO_0021166"},{"id":"A7","pred":"mondo_id","subj":"T7","obj":"http://purl.obolibrary.org/obo/MONDO_0005098"},{"id":"A8","pred":"mondo_id","subj":"T7","obj":"http://purl.obolibrary.org/obo/MONDO_0011057"},{"id":"A9","pred":"mondo_id","subj":"T9","obj":"http://purl.obolibrary.org/obo/MONDO_0021166"},{"id":"A10","pred":"mondo_id","subj":"T10","obj":"http://purl.obolibrary.org/obo/MONDO_0005098"},{"id":"A11","pred":"mondo_id","subj":"T10","obj":"http://purl.obolibrary.org/obo/MONDO_0011057"}],"text":"Soluble epoxide hydrolase as an anti-inflammatory target of the thrombolytic stroke drug SMTP-7.\nAlthough ischemic stroke is a major cause of death and disability worldwide, only a small fraction of patients benefit from the current thrombolytic therapy due to a risk of cerebral hemorrhage caused by inflammation. Thus, the development of a new strategy to combat inflammation during thrombolysis is an urgent demand. The small molecule thrombolytic SMTP-7 effectively treats ischemic stroke in several animal models with reducing cerebral hemorrhage. Here we revealed that SMTP-7 targeted soluble epoxide hydrolase (sEH) to suppress inflammation. SMTP-7 inhibited both of the two sEH enzyme activities: epoxide hydrolase (which inactivates anti-inflammatory epoxy-fatty acids) and lipid phosphate phosphatase. SMTP-7 suppressed epoxy-fatty acid hydrolysis in HepG2 cells in culture, implicating the sEH inhibition in the anti-inflammatory mechanism. The sEH inhibition by SMTP-7 was independent of its thrombolytic activity. The simultaneous targeting of thrombolysis and sEH by a single molecule is a promising strategy to revolutionize the current stroke therapy."}
HP-phenotype
{"project":"HP-phenotype","denotations":[{"id":"T1","span":{"begin":77,"end":83},"obj":"Phenotype"},{"id":"T2","span":{"begin":106,"end":121},"obj":"Phenotype"},{"id":"T3","span":{"begin":271,"end":290},"obj":"Phenotype"},{"id":"T4","span":{"begin":477,"end":492},"obj":"Phenotype"},{"id":"T5","span":{"begin":532,"end":551},"obj":"Phenotype"},{"id":"T6","span":{"begin":1152,"end":1158},"obj":"Phenotype"}],"attributes":[{"id":"A1","pred":"hp_id","subj":"T1","obj":"HP:0001297"},{"id":"A2","pred":"hp_id","subj":"T2","obj":"HP:0002140"},{"id":"A3","pred":"hp_id","subj":"T3","obj":"HP:0001342"},{"id":"A4","pred":"hp_id","subj":"T4","obj":"HP:0002140"},{"id":"A5","pred":"hp_id","subj":"T5","obj":"HP:0001342"},{"id":"A6","pred":"hp_id","subj":"T6","obj":"HP:0001297"}],"namespaces":[{"prefix":"HP","uri":"http://purl.obolibrary.org/obo/HP_"}],"text":"Soluble epoxide hydrolase as an anti-inflammatory target of the thrombolytic stroke drug SMTP-7.\nAlthough ischemic stroke is a major cause of death and disability worldwide, only a small fraction of patients benefit from the current thrombolytic therapy due to a risk of cerebral hemorrhage caused by inflammation. Thus, the development of a new strategy to combat inflammation during thrombolysis is an urgent demand. The small molecule thrombolytic SMTP-7 effectively treats ischemic stroke in several animal models with reducing cerebral hemorrhage. Here we revealed that SMTP-7 targeted soluble epoxide hydrolase (sEH) to suppress inflammation. SMTP-7 inhibited both of the two sEH enzyme activities: epoxide hydrolase (which inactivates anti-inflammatory epoxy-fatty acids) and lipid phosphate phosphatase. SMTP-7 suppressed epoxy-fatty acid hydrolysis in HepG2 cells in culture, implicating the sEH inhibition in the anti-inflammatory mechanism. The sEH inhibition by SMTP-7 was independent of its thrombolytic activity. The simultaneous targeting of thrombolysis and sEH by a single molecule is a promising strategy to revolutionize the current stroke therapy."}