FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2191736894> ?p ?o ?g. }

• W2191736894 endingPage "e491" @default.
• W2191736894 startingPage "e477" @default.
• W2191736894 abstract "Objective: Vascular dysfunction such as vascular hyporeactivity following severe trauma and shock is a major cause of death in injured patients. Oxidative stress and endoplasmic reticulum stress play an important role in vascular dysfunction. The objective of the present study was to determine whether or not 4-phenylbutyrate can improve vascular dysfunction and elicit antishock effects by inhibiting oxidative and endoplasmic reticulum stress. Design: Prospective, randomized, controlled laboratory experiment. Setting: State key laboratory of trauma, burns, and combined injury. Subjects: Five hundred and fifty-two Sprague-Dawley rats. Interventions: Rats were anesthetized, and a model of traumatic hemorrhagic shock was established by left femur fracture and hemorrhage. The effects of 4-phenylbutyrate (5, 20, 50, 100, 200, and 300 mg/kg) on vascular reactivity, animal survival, hemodynamics, and vital organ function in traumatic hemorrhagic shock rats and cultured vascular smooth muscle cells, and the relationship to oxidative stress and endoplasmic reticulum stress was observed. Measurements and Main Results: Lower doses of 4-phenylbutyrate significantly improved the vascular function, stabilized the hemodynamics, and increased the tissue blood flow and vital organ function in traumatic hemorrhagic shock rats, and markedly improved the survival outcomes. Among all dosages observed in the present study, 20 mg/kg of 4-phenylbutyrate had the best effect. Further results indicated that 4-phenylbutyrate significantly inhibited the oxidative stress, decreased shock-induced oxidative stress index such as the production of reactive oxygen species, increased the antioxidant enzyme levels such as superoxide dismutase, catalase, and glutathione, and improved the mitochondrial function by inhibiting the opening of the mitochondrial permeability transition pore in rat artery and vascular smooth muscle cells. In contrast, 4-phenylbutyrate did not affect the changes of endoplasmic reticulum stress markers following traumatic hemorrhagic shock. Furthermore, 4-phenylbutyrate increased the nuclear levels of nuclear factor-E2–related factor 2, and decreased the nuclear levels of nuclear factor κB in hypoxic vascular smooth muscle cells. Conclusions: 4-phenylbutyrate has beneficial effects for traumatic hemorrhagic shock including improving animal survival and protecting organ function. These beneficial effects of 4-phenylbutyrate in traumatic hemorrhagic shock result from its vascular function protection via attenuation of the oxidative stress and mitochondrial permeability transition pore opening. Nuclear factor-E2–related factor 2 and nuclear factor-κB may be involved in 4-phenylbutyrate-mediated inhibition of oxidative stress." @default.
• W2191736894 created "2016-06-24" @default.
• W2191736894 creator A5007602246 @default.
• W2191736894 creator A5014054701 @default.
• W2191736894 creator A5017069269 @default.
• W2191736894 creator A5047421180 @default.
• W2191736894 creator A5055987578 @default.
• W2191736894 creator A5061987021 @default.
• W2191736894 creator A5086326013 @default.
• W2191736894 date "2016-07-01" @default.
• W2191736894 modified "2023-09-23" @default.
• W2191736894 title "4-Phenylbutyrate Benefits Traumatic Hemorrhagic Shock in Rats by Attenuating Oxidative Stress, Not by Attenuating Endoplasmic Reticulum Stress" @default.
• W2191736894 cites W1582375112 @default.
• W2191736894 cites W1753629688 @default.
• W2191736894 cites W1814756288 @default.
• W2191736894 cites W1965443388 @default.
• W2191736894 cites W1970421321 @default.
• W2191736894 cites W1973531470 @default.
• W2191736894 cites W1974942333 @default.
• W2191736894 cites W1988749527 @default.
• W2191736894 cites W1991465901 @default.
• W2191736894 cites W1995787281 @default.
• W2191736894 cites W1997288864 @default.
• W2191736894 cites W2000410859 @default.
• W2191736894 cites W2006441888 @default.
• W2191736894 cites W2010206750 @default.
• W2191736894 cites W2013103361 @default.
• W2191736894 cites W2013958980 @default.
• W2191736894 cites W2024870847 @default.
• W2191736894 cites W2029042746 @default.
• W2191736894 cites W2029513164 @default.
• W2191736894 cites W2033450092 @default.
• W2191736894 cites W2034459537 @default.
• W2191736894 cites W2037082103 @default.
• W2191736894 cites W2038109543 @default.
• W2191736894 cites W2038984648 @default.
• W2191736894 cites W2057495929 @default.
• W2191736894 cites W2059031625 @default.
• W2191736894 cites W2062354893 @default.
• W2191736894 cites W2066335949 @default.
• W2191736894 cites W2085025210 @default.
• W2191736894 cites W2090384427 @default.
• W2191736894 cites W2108339719 @default.
• W2191736894 cites W2120284592 @default.
• W2191736894 cites W2142981758 @default.
• W2191736894 cites W2144827966 @default.
• W2191736894 cites W2154838463 @default.
• W2191736894 cites W2160054528 @default.
• W2191736894 cites W2162349906 @default.
• W2191736894 cites W2167381526 @default.
• W2191736894 cites W2168868325 @default.
• W2191736894 cites W2169135796 @default.
• W2191736894 cites W2313177501 @default.
• W2191736894 cites W2321805476 @default.
• W2191736894 cites W2327787929 @default.
• W2191736894 cites W2333829012 @default.
• W2191736894 cites W3023757607 @default.
• W2191736894 doi "https://doi.org/10.1097/ccm.0000000000001469" @default.
• W2191736894 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26646458" @default.
• W2191736894 hasPublicationYear "2016" @default.
• W2191736894 type Work @default.
• W2191736894 sameAs 2191736894 @default.
• W2191736894 citedByCount "14" @default.
• W2191736894 countsByYear W21917368942016 @default.
• W2191736894 countsByYear W21917368942018 @default.
• W2191736894 countsByYear W21917368942019 @default.
• W2191736894 countsByYear W21917368942020 @default.
• W2191736894 countsByYear W21917368942021 @default.
• W2191736894 countsByYear W21917368942023 @default.
• W2191736894 crossrefType "journal-article" @default.
• W2191736894 hasAuthorship W2191736894A5007602246 @default.
• W2191736894 hasAuthorship W2191736894A5014054701 @default.
• W2191736894 hasAuthorship W2191736894A5017069269 @default.
• W2191736894 hasAuthorship W2191736894A5047421180 @default.
• W2191736894 hasAuthorship W2191736894A5055987578 @default.
• W2191736894 hasAuthorship W2191736894A5061987021 @default.
• W2191736894 hasAuthorship W2191736894A5086326013 @default.
• W2191736894 hasConcept C126322002 @default.
• W2191736894 hasConcept C134018914 @default.
• W2191736894 hasConcept C158617107 @default.
• W2191736894 hasConcept C185592680 @default.
• W2191736894 hasConcept C2775838275 @default.
• W2191736894 hasConcept C2776151105 @default.
• W2191736894 hasConcept C2778401633 @default.
• W2191736894 hasConcept C2781300812 @default.
• W2191736894 hasConcept C2909310144 @default.
• W2191736894 hasConcept C55493867 @default.
• W2191736894 hasConcept C71924100 @default.
• W2191736894 hasConcept C98274493 @default.
• W2191736894 hasConceptScore W2191736894C126322002 @default.
• W2191736894 hasConceptScore W2191736894C134018914 @default.
• W2191736894 hasConceptScore W2191736894C158617107 @default.
• W2191736894 hasConceptScore W2191736894C185592680 @default.
• W2191736894 hasConceptScore W2191736894C2775838275 @default.
• W2191736894 hasConceptScore W2191736894C2776151105 @default.
• W2191736894 hasConceptScore W2191736894C2778401633 @default.
• W2191736894 hasConceptScore W2191736894C2781300812 @default.
• W2191736894 hasConceptScore W2191736894C2909310144 @default.

• next