FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2947694448> ?p ?o ?g. }

• W2947694448 endingPage "15" @default.
• W2947694448 startingPage "1" @default.
• W2947694448 abstract "The present study was conducted to investigate the effect and potential mechanism of hypoxia-inducible factor-1 α (HIF-1 α ) genetic inhibition plus glutamine (Gln) supplementation on necrosis-apoptosis imbalance during acute pancreatitis (AP), with a specific focus on the regulations of intracellular energy metabolism status. Wistar rats and AR42J cells were used to establish AP models. When indicated, a HIF-1 α knockdown with or without a Gln supplementation was administered. In vivo , local and systemic inflammatory injuries were assessed by serum cytokine measurement, H&E staining, and transmission electron microscope (TEM) observation of pancreatic tissue. In vitro , intracellular energy metabolism status was evaluated by measuring the intracellular adenosine triphosphate (ATP), lactic acid, and Ca 2+ concentrations and the mitochondrial potential. In addition, changes in the apoptotic activity were analyzed using TUNEL staining in vivo and an apoptosis assay in vitro. HIF-1 α knockdown alleviated AP-related inflammatory injury as indicated by the measurements of serum cytokines and examinations of TEM and H&E staining of pancreatic tissues. HIF-1 α knockdown played an antioxidative role against AP-related injuries by preventing the increase in the intracellular Ca 2+ concentration and the decrease in the mitochondrial membrane potential and subsequently by suppressing the glycolysis pathway and increasing energy anabolism in AR42J cells after AP induction. Apoptosis was significantly upregulated when HIF-1 α was knocked down before AP induction due to an attenuation of the translocation of nuclear factor-kappa B to the nuclei. Furthermore, these merits of HIF-1 α knockdown in the relief of the metabolic stress and upregulation of apoptosis were more significant when Gln was administered concomitantly. In conclusion, Gln-supplemented HIF-1 α knockdown might be promising for the future management of AP by relieving the intracellular energy stress, thereby attenuating the predominance of necrosis over apoptosis." @default.
• W2947694448 created "2019-06-07" @default.
• W2947694448 creator A5004810018 @default.
• W2947694448 creator A5005582179 @default.
• W2947694448 creator A5012806139 @default.
• W2947694448 creator A5014346457 @default.
• W2947694448 creator A5028097742 @default.
• W2947694448 creator A5055896550 @default.
• W2947694448 creator A5076528747 @default.
• W2947694448 creator A5085073387 @default.
• W2947694448 creator A5090572585 @default.
• W2947694448 date "2019-06-02" @default.
• W2947694448 modified "2023-10-18" @default.
• W2947694448 title "Hypoxia-Inducible Factor-1<i>α</i>Knockdown Plus Glutamine Supplementation Attenuates the Predominance of Necrosis over Apoptosis by Relieving Cellular Energy Stress in Acute Pancreatitis" @default.
• W2947694448 cites W1500939659 @default.
• W2947694448 cites W1607531254 @default.
• W2947694448 cites W1900078466 @default.
• W2947694448 cites W1966849251 @default.
• W2947694448 cites W1969640807 @default.
• W2947694448 cites W1970070807 @default.
• W2947694448 cites W1973564461 @default.
• W2947694448 cites W1990664796 @default.
• W2947694448 cites W1991346678 @default.
• W2947694448 cites W1996024251 @default.
• W2947694448 cites W1997070121 @default.
• W2947694448 cites W1999375802 @default.
• W2947694448 cites W2003030880 @default.
• W2947694448 cites W2009841576 @default.
• W2947694448 cites W2010322339 @default.
• W2947694448 cites W2014866968 @default.
• W2947694448 cites W2015426350 @default.
• W2947694448 cites W2016553156 @default.
• W2947694448 cites W2016601308 @default.
• W2947694448 cites W2022155885 @default.
• W2947694448 cites W2027994201 @default.
• W2947694448 cites W2028191514 @default.
• W2947694448 cites W2034429828 @default.
• W2947694448 cites W2035693999 @default.
• W2947694448 cites W2048762049 @default.
• W2947694448 cites W2054386531 @default.
• W2947694448 cites W2055388969 @default.
• W2947694448 cites W2055902411 @default.
• W2947694448 cites W2056988473 @default.
• W2947694448 cites W2061987997 @default.
• W2947694448 cites W2065276651 @default.
• W2947694448 cites W2070278049 @default.
• W2947694448 cites W2070603331 @default.
• W2947694448 cites W2073499403 @default.
• W2947694448 cites W2073706613 @default.
• W2947694448 cites W2080561368 @default.
• W2947694448 cites W2085687807 @default.
• W2947694448 cites W2087814592 @default.
• W2947694448 cites W2091106134 @default.
• W2947694448 cites W2104263620 @default.
• W2947694448 cites W2111911031 @default.
• W2947694448 cites W2113689677 @default.
• W2947694448 cites W2117674153 @default.
• W2947694448 cites W2122310415 @default.
• W2947694448 cites W2131467340 @default.
• W2947694448 cites W2133669258 @default.
• W2947694448 cites W2134160865 @default.
• W2947694448 cites W2134287168 @default.
• W2947694448 cites W2141260882 @default.
• W2947694448 cites W2154763401 @default.
• W2947694448 cites W2161899812 @default.
• W2947694448 cites W2165048131 @default.
• W2947694448 cites W2171493598 @default.
• W2947694448 cites W2208468048 @default.
• W2947694448 cites W2334714409 @default.
• W2947694448 cites W2428978411 @default.
• W2947694448 cites W2474601986 @default.
• W2947694448 cites W2614360956 @default.
• W2947694448 cites W4211022384 @default.
• W2947694448 doi "https://doi.org/10.1155/2019/4363672" @default.
• W2947694448 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6589200" @default.
• W2947694448 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31281575" @default.
• W2947694448 hasPublicationYear "2019" @default.
• W2947694448 type Work @default.
• W2947694448 sameAs 2947694448 @default.
• W2947694448 citedByCount "6" @default.
• W2947694448 countsByYear W29476944482021 @default.
• W2947694448 countsByYear W29476944482022 @default.
• W2947694448 countsByYear W29476944482023 @default.
• W2947694448 crossrefType "journal-article" @default.
• W2947694448 hasAuthorship W2947694448A5004810018 @default.
• W2947694448 hasAuthorship W2947694448A5005582179 @default.
• W2947694448 hasAuthorship W2947694448A5012806139 @default.
• W2947694448 hasAuthorship W2947694448A5014346457 @default.
• W2947694448 hasAuthorship W2947694448A5028097742 @default.
• W2947694448 hasAuthorship W2947694448A5055896550 @default.
• W2947694448 hasAuthorship W2947694448A5076528747 @default.
• W2947694448 hasAuthorship W2947694448A5085073387 @default.
• W2947694448 hasAuthorship W2947694448A5090572585 @default.
• W2947694448 hasBestOaLocation W29476944481 @default.
• W2947694448 hasConcept C126322002 @default.
• W2947694448 hasConcept C173396325 @default.
• W2947694448 hasConcept C190283241 @default.
• W2947694448 hasConcept C196795494 @default.

• next