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10.18632/oncotarget.12119 http://scihub22266oqcxt.onion/10.18632/oncotarget.12119 C5341812!5341812 !27661104     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27661104 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27661104 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Oncotarget 2016 ; 7 (41 ): 66444-66454 Nephropedia Template TP {{tp|p=27661104 |t=2016. ?-Hydroxybutyrate suppresses inflammasome formation by ameliorating endoplasmic reticulum stress via AMPK activation |pdf=|usr=}}{{27661104 }} gab.com Text -Hydroxybutyrate suppresses inflammasome formation by ameliorating endoplasmic reticulum stress via AMPK activation JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27661104 #FOAvip ?-Hydroxybutyrate, a ketone body that is used as an energy source in organs such as the brain, muscle, and heart when blood glucose is low, is produced by fatty acid oxidation in the liver under the fasting state. Endoplasmic reticulum (ER) stress is linked with the generation of intracellular reactive oxygen species and the accumulation of misfolded protein in the ER. ER stress is known to induce the NOD-like receptor protein 3 inflammasome, which mediates activation of the proinflammatory cytokine interleukin-1?, whose maturation is caspase-1-dependent. We investigated whether ?-hydroxybutyrate modulates ER stress, inflammasome formation, and insulin signaling. Sprague Dawley rats (6 and 24 months of age) that were starved for 3 d and rats treated with ?-hydroxybutyrate (200 mg·kg-1·d-1 i.p., for 5 d) were used for in vivo investigations, whereas human hepatoma HepG2 cells were used for in vitro studies. Overexpression of AMPK in cultured cells was performed to elucidate the molecular mechanism. The starvation resulted in increased serum ?-hydroxybutyrate levels with decreased ER stress (PERK, IRE1, and ATF6?) and inflammasome (ASC, caspase-1, and NLRP3) formation compared with non-fasted 24-month-old rats. In addition, ?-hydroxybutyrate suppressed the increase of ER stress- and inflammasome-related marker proteins. Furthermore, ?-hydroxybutyrate treatment increased the expression of manganese superoxide dismutase and catalase via the AMP-activated protein kinase-forkhead box protein O3? transcription factor pathway both in vivo and in vitro. The significance of the current study was the discovery of the potential therapeutic role of ?-hydroxybutyrate in suppressing ER-stress-induced inflammasome formation. Twit Text FOAVip -Hydroxybutyrate suppresses inflammasome formation by ameliorating endoplasmic reticulum stress via AMPK activation ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27661104 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27661104 #FOAvip English Wikipedia <ref>{{Cite pmid|27661104 }}</ref> ?-Hydroxybutyrate suppresses inflammasome formation by ameliorating endoplasmic reticulum stress via AMPK activation #MMPMID27661104 Bae HR ; Kim DH ; Park MH ; Lee B ; Kim MJ ; Lee EK ; Chung KW ; Kim SM ; Im DS ; Chung HY Oncotarget 2016[Oct]; 7 (41 ): 66444-66454 PMID27661104 show ga ?-Hydroxybutyrate, a ketone body that is used as an energy source in organs such as the brain, muscle, and heart when blood glucose is low, is produced by fatty acid oxidation in the liver under the fasting state. Endoplasmic reticulum (ER) stress is linked with the generation of intracellular reactive oxygen species and the accumulation of misfolded protein in the ER. ER stress is known to induce the NOD-like receptor protein 3 inflammasome, which mediates activation of the proinflammatory cytokine interleukin-1?, whose maturation is caspase-1-dependent. We investigated whether ?-hydroxybutyrate modulates ER stress, inflammasome formation, and insulin signaling. Sprague Dawley rats (6 and 24 months of age) that were starved for 3 d and rats treated with ?-hydroxybutyrate (200 mg·kg-1·d-1 i.p., for 5 d) were used for in vivo investigations, whereas human hepatoma HepG2 cells were used for in vitro studies. Overexpression of AMPK in cultured cells was performed to elucidate the molecular mechanism. The starvation resulted in increased serum ?-hydroxybutyrate levels with decreased ER stress (PERK, IRE1, and ATF6?) and inflammasome (ASC, caspase-1, and NLRP3) formation compared with non-fasted 24-month-old rats. In addition, ?-hydroxybutyrate suppressed the increase of ER stress- and inflammasome-related marker proteins. Furthermore, ?-hydroxybutyrate treatment increased the expression of manganese superoxide dismutase and catalase via the AMP-activated protein kinase-forkhead box protein O3? transcription factor pathway both in vivo and in vitro. The significance of the current study was the discovery of the potential therapeutic role of ?-hydroxybutyrate in suppressing ER-stress-induced inflammasome formation. |3-Hydroxybutyric Acid/*pharmacology [MESH] |AMP-Activated Protein Kinases/*metabolism [MESH] |Animals [MESH] |Endoplasmic Reticulum Stress/*drug effects/physiology [MESH] |Enzyme Activation/drug effects [MESH] |Hep G2 Cells [MESH] |Humans [MESH] |Inflammasomes/*drug effects [MESH] |Male [MESH] |Rats [MESH]?-Hydroxybutyrate suppresses inflammasome formation by ameliorating en(epmc).pdf DeepDyve Pubget Overpricing