title: Powerful protection against renal ischemia reperfusion injury by T cell-specific NF-κB inhibition.
abstract: BACKGROUND
  NF-κB plays a key role in ischemia reperfusion injury (IRI). Systemic inhibition of NF-κB by various methods has been proven to ameliorate IRI. However, NF-κB is also responsible for tissue protection against IRI. Systemic NF-κB inhibition may not be the optimal way for preventing IRI because of its complex roles. T cells are essential in mediating IRI. NF-κB is an important molecule during T cell activation. It is not clear the effect of T cell-specific NF-κB inhibition on IRI. We aimed to study the effect of T cell-specific NF-κB inhibition on renal IRI in IκBαΔN-Tg mice. We also compared the different effects between T cell-specific and systemic NF-κB inhibition on IRI.
  
  
  METHODS
  Renal IRI was induced by left renal pedicle clamping for 60 or 80 min in wild-type, ursolic acid-treated or IκBαΔN-Tg mice. Renal function, histologic examination and overall survival after lethal IRI was evaluated in each group.
  
  
  RESULTS
  Serum creatinine, BUN, and pathologic damage were all reduced in IκBαDN-Tg mice and ursolic acid-treated mice than those in the control group. All the above indexes were improved better in IκBαDN-Tg mice than those in ursolic acid-treated mice. The survival rate of IκBαDN-Tg mice was higher than that of ursolic acid-treated mice after lethal kidney ischemia reperfusion injury. Immunohistochemistry showed a significant reduced CD4+ T cells and neutrophil infiltration in IκBαDN-Tg mice.
  
  
  CONCLUSIONS
  T cell-specific NF-κB inhibition provides powerful protective effect against renal IRI.
authors.affiliation: 1 Institute of Organ Transplantation, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Key Laboratory of Ministry of Health, and Key Laboratory of Ministry of Education, China. 2 Department of Anesthesiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. 3 Address correspondence to: Ping Zhou, 1095 Jiefang Road, Tongji Hospital, Institute of Organ Transplantation, Wuhan, Hubei 430030, China.
authors.forename: ChengBiao
authors.initials: C
authors.lastname: Xue
authors.forename: Yong
authors.initials: Y
authors.lastname: Liu
authors.forename: Chao
authors.initials: C
authors.lastname: Li
authors.forename: Yao
authors.initials: Y
authors.lastname: Li
authors.forename: Tao
authors.initials: T
authors.lastname: Yang
authors.forename: Lin
authors.initials: L
authors.lastname: Xie
authors.forename: Ping
authors.initials: P
authors.lastname: Zhou
mesh_terms: D000818:Animals; D001806:Blood Urea Nitrogen; D015496:CD4-Positive T-Lymphocytes / Q000166:cytology / Q000378:metabolism / Q000473:pathology*; D003404:Creatinine / Q000097:blood; D016207:Cytokines / Q000378:metabolism; D007150:Immunohistochemistry; D007249:Inflammation; D007668:Kidney / Q000378:metabolism / Q000473:pathology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D016328:NF-kappa B / Q000037:antagonists & inhibitors* / Q000378:metabolism*; D020556:Neutrophil Infiltration; D009504:Neutrophils / Q000378:metabolism; D060888:Real-Time Polymerase Chain Reaction; D015427:Reperfusion Injury / Q000517:prevention & control*; D013997:Time Factors; D014315:Triterpenes / Q000737:chemistry; D000097245:Ursolic Acid
chemical_list: D003404:Creatinine; D016207:Cytokines; D016328:NF-kappa B; D014315:Triterpenes; D000097245:Ursolic Acid