title: Altered miR-370 expression in hepatic ischemia-reperfusion injury correlates with the level of nuclear kappa B (NF-κB) related factors.
abstract: OBJECTIVE
  MicroRNAs (miRNAs) are a class of small endogenous, non-coding RNAs that regulate gene expression at both the transcription and translation levels. Whether miRNAs have taken part in liver ischemia-reperfusion (IR) injury was rarely reported. The purpose of this article is to investigate the potential role of miR-370 in hepatic IR injury.
  
  
  METHODS
  Male C57BL/6 mice were divided into 5 groups (sham-operated group, I/R group, IPC group, antagomir-370 group and antagomir-NC), and the expression levels of miR-370 were assessed by quantitative real-time PCR. Serum enzyme analysis and histological examination of liver were used as the index of the effect of miR-370 on hepatic IR injury and following treatment of mice with antagomir-370 or antagomir-NC. The classical pathway factors of NF-κB (TAK1, TAB1, TAB2, IkBα, IKKα, IKKβ, p50, p65) were studied by quantitative real-time PCR and Western blot.
  
  
  RESULTS
  The results showed that the IR group's miR-370 expression level was significantly upregulated as compared with the sham-operated group and IPC group. Also inhibition of miR-370 led to the low expression levels of miR-370 and low levels of serum aminotransferase and hepatic histological damage as compared with the IR group. Quantitative real-time PCR showed the levels of TAK1, TAB1, TAB2, IkBα, IKKα, p65 was elevated when improving the miR-370 levels, at the same time, Western blot showed the levels of TAK1, TAB1, TAB2, IkBα, IKKα, IKKβ, p50, p65 were all elevated.
  
  
  CONCLUSIONS
  miR-370 acting via NF-κB might play a crucial role in hepatic IR injury, and inhibition of miR-370 could alleviate the injury to the liver. And miR-370 might positively regulated the NF-κB pathway.
authors.affiliation: College of Medicine, Ningbo University, China.
authors.forename: Jie
authors.initials: J
authors.lastname: Zhu
authors.affiliation: Ningbo Medical Centre of LIHuiLi Hospital, China.
authors.forename: Fangfang
authors.initials: F
authors.lastname: Zhu
authors.affiliation: The First Affiliated Hospital, College Of Medicine, Zhejiang University.
authors.forename: Wenfeng
authors.initials: W
authors.lastname: Song
authors.affiliation: Ningbo Medical Centre of LIHuiLi Hospital, China.
authors.forename: Bin
authors.initials: B
authors.lastname: Zhang
authors.affiliation: Ningbo Medical Centre of LIHuiLi Hospital, China.
authors.forename: Xie
authors.initials: X
authors.lastname: Zhang
authors.affiliation: College of Medicine, Fudan University.
authors.forename: Xiaofeng
authors.initials: X
authors.lastname: Jin
authors.affiliation: Ningbo Medical Centre of LIHuiLi Hospital, China. Electronic address: 1411101252@nbu.edu.cn.
authors.forename: Hong
authors.initials: H
authors.lastname: Li
mesh_terms: D000818:Animals; D005786:Gene Expression Regulation; D007511:Ischemia / Q000235:genetics / Q000378:metabolism*; D008099:Liver / Q000098:blood supply* / Q000378:metabolism / Q000473:pathology; D008297:Male; D008810:Mice, Inbred C57BL; D035683:MicroRNAs / Q000235:genetics*; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism*; D015427:Reperfusion Injury / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction
chemical_list: C551449:MIRN370 microRNA, mouse; D035683:MicroRNAs; D016328:NF-kappa B
keywords: Injury; Ischemia-reperfusion; Liver; NF-κB; miR-370