title: rhTNFR:Fc increases Nrf2 expression via miR-27a mediation to protect myocardium against sepsis injury.
abstract: OBJECTIVE
  Sepsis is a whole-body inflammation disease and can result in septic shock and multiple organ failure. The previous study demonstrated that miR-27a plays a critical role in inflammation regulation. Here, we investigated that effect and its possible mechanism of rhTNFR:Fc on sepsis treatment.
  
  
  METHODS
  LPS induced sepsis mice model was established. 10 mg/kg rhTNFR:Fc was used to treat sepsis mice by intravenous injection.
  
  
  RESULTS
  RhTNFR:Fc improved cardiac function of sepsis mice, and markedly decreased miR-27a but increased Nrf2 expression level of myocardium in LPS treated mice. In H9C2 cells, rhTNFR:Fc also increased Nrf2 expression, elevated cell viability and decreased cell apoptosis. However, the effects were reversed by miR-27a mimic. In addition, miR-27a mimic reduced the activity of Nrf2 3'UTR while miR-27a inhibitor elevated enhanced its level.
  
  
  CONCLUSIONS
  rhTNFR:Fc activated Nrf2 pathway to protect myocardium against LPS-induced sepsis injury via miR-27a regulation.
authors.affiliation: Department of Emergency, The People's Hospital of the Ningxia Hui Autonomous Region, Yinchuan 750000, China. Electronic address: weiliang968@163.com.
authors.forename: Wei-Liang
authors.initials: WL
authors.lastname: Xue
authors.affiliation: Division of Nephrology, Nanfang Hospital, Southern Medical University, National Clinical Medical Research Center for Kidney Disease, National Key Lab for Organ Failure Research, Guangdong Provincial Institute of Nephrology, Guangzhou 510515, China.
authors.forename: Xiaoyan
authors.initials: X
authors.lastname: Bai
authors.affiliation: Department of Emergency, The People's Hospital of the Ningxia Hui Autonomous Region, Yinchuan 750000, China.
authors.forename: Ling
authors.initials: L
authors.lastname: Zhang
mesh_terms: D020413:3' Untranslated Regions; D000818:Animals; D002316:Cardiotonic Agents / Q000494:pharmacology*; D002478:Cells, Cultured; D000068800:Etanercept; D005786:Gene Expression Regulation / Q000187:drug effects; D006321:Heart / Q000187:drug effects* / Q000503:physiopathology; D007074:Immunoglobulin G / Q000235:genetics / Q000378:metabolism / Q000494:pharmacology*; D008070:Lipopolysaccharides / Q000633:toxicity; D008297:Male; D008810:Mice, Inbred C57BL; D035683:MicroRNAs / Q000235:genetics / Q000378:metabolism*; D032386:Myoblasts, Cardiac / Q000187:drug effects / Q000473:pathology; D051267:NF-E2-Related Factor 2 / Q000235:genetics / Q000378:metabolism*; D051381:Rats; D018124:Receptors, Tumor Necrosis Factor / Q000235:genetics / Q000378:metabolism; D018805:Sepsis / Q000188:drug therapy* / Q000235:genetics / Q000503:physiopathology
chemical_list: D020413:3' Untranslated Regions; D002316:Cardiotonic Agents; D007074:Immunoglobulin G; D008070:Lipopolysaccharides; C531388:MIRN27 microRNA, human; C000594049:MIRN27 microRNA, rat; D035683:MicroRNAs; D051267:NF-E2-Related Factor 2; C495636:Nfe2l2 protein, mouse; C495637:Nfe2l2 protein, rat; D018124:Receptors, Tumor Necrosis Factor; D000068800:Etanercept
keywords: Nrf2; Sepsis; miR-27a; rhTNFR:Fc