title: [Effect of UCP2-siRNA on inflammatory response of cardiomyocytes induced by septic serum].
abstract: OBJECTIVE
  To study the effect of uncoupling protein 2 (UCP2)-siRNA on the inflammatory response of rat cardiomyocytes (H9C2) induced by septic serum and to investigate the possible role of UCP2 in the development of septic cardiomyopathy.
  
  
  METHODS
  Serum samples were separately collected from normal rats and septic rats. Cultured rat cardiac cells (H9C2) were randomly divided into blank control, normal serum, 10% septic serum, UCP2-siRNA+10% septic serum and negative siRNA+10% septic serum groups. Stimulation with 10% septic serum was performed for 12 hours in relevant groups. The mRNA expression of tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β) was measured by RT-PCR. The expression of phosphorylated p38 mitogen-activated protein kinase (p-p38 MAPK) and nuclear factor-kappa B (NF-κB) was measured by Western blot.
  
  
  RESULTS
  The expression levels of p-p38 and NF-κB in the UCP2-siRNA+10% septic serum group were significantly higher than in the 10% septic serum group (P<0.05). The UCP2-siRNA+10% septic serum group had a significantly higher TNF-α mRNA expression than the 10% septic serum group (P<0.01), but IL-1β mRNA expression showed no significant difference between the two groups.
  
  
  CONCLUSIONS
  UCP2 plays a regulatory role in the activation of p38 MAPK and NF-κB and the expression of downstream inflammatory mediators in H9C2 cells stimulated with septic serum.
authors.affiliation: Pediatric Center of Zhujiang Hospital, Southern Medical University, Guangzhou 510282, China. zqy_88@163.com.
authors.forename: Zhi-Jiang
authors.initials: ZJ
authors.lastname: Chen
authors.forename: Yuan-Bin
authors.initials: YB
authors.lastname: Song
authors.forename: Hui-Li
authors.initials: HL
authors.lastname: Wang
authors.forename: Yang
authors.initials: Y
authors.lastname: Wang
authors.forename: Juan-Juan
authors.initials: JJ
authors.lastname: Lv
authors.forename: Di
authors.initials: D
authors.lastname: Che
authors.forename: Qi-Yi
authors.initials: QY
authors.lastname: Zeng
mesh_terms: D000818:Animals; D009202:Cardiomyopathies / Q000209:etiology*; D002478:Cells, Cultured; D007249:Inflammation / Q000209:etiology*; D053583:Interleukin-1beta / Q000235:genetics; D007473:Ion Channels / Q000235:genetics / Q000502:physiology*; D008297:Male; D024101:Mitochondrial Proteins / Q000235:genetics / Q000502:physiology*; D032383:Myocytes, Cardiac / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D034741:RNA, Small Interfering / Q000235:genetics*; D051381:Rats; D017207:Rats, Sprague-Dawley; D018805:Sepsis / Q000097:blood / Q000150:complications*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics; D000071246:Uncoupling Protein 2; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
chemical_list: D053583:Interleukin-1beta; D007473:Ion Channels; D024101:Mitochondrial Proteins; D016328:NF-kappa B; D034741:RNA, Small Interfering; D014409:Tumor Necrosis Factor-alpha; C000604391:Ucp2 protein, rat; D000071246:Uncoupling Protein 2; D048051:p38 Mitogen-Activated Protein Kinases