title: [Effect of ubiquitin-proteasome pathway on inflammatory reaction in intestine and its barrier function in rats with postburn sepsis].
abstract: OBJECTIVE
  To study the effect of ubiquitin-proteasome pathway inhibition on intestinal nuclear factor-KappaB (NF-KappaB) activity and tumor necrosis factor-alpha (TNF-alpha) release as well as plasma diamine oxidase (DAO) activity in rats with postburn sepsis.
  
  
  METHODS
  Rats were subjected to 30% total body surface area (TBSA) full-thickness scald injury, followed by intraperitoneal injection of lipopolysaccharide (LPS) to mimic postburn sepsis. Sixty Wistar rats were randomly divided into normal control group, sepsis group, sepsis with proteasome inhibitor N-Acetyl leucinyl leucinyl norleucinal (ALLN) treatment group and sepsis with NF-KappaB inhibitor pyrrolidine dithiocarbamate (PDTC) treatment group. NF-KappaB activity, TNF-alpha protein content, and plasma DAO activity were determined by electrophoretic mobility shift assay (EMSA), enzyme-linked immunosorbent assay (ELISA), and spectrophotometric method, respectively.
  
  
  RESULTS
  The results showed that NF-KappaB activity was markedly activated and reached its peak 1 hour after scalding and injection of LPS in each group (all P<0.01), then reduced gradually. Both ALLN and PDTC could decrease intestinal NF-KappaB activity at 1 hour and 2 hours after injury. TNF-alpha release was reduced by ALLN at 1 hour after injury (P<0.01). Plasma DAO activity was significantly elevated after scalding and injection of LPS (P<0.01). Pretreatment with PDTC or ALLN could not lower the activity of DAO.
  
  
  CONCLUSIONS
  The results suggest that early treatment with inhibitor of ubiquitin-proteasome pathway might decrease the intestinal inflammatory reaction, but exert no effect on intestinal barrier function in rats with postburn sepsis.
authors.affiliation: First Hospital Affiliated to the General Hospital of PLA (formerly 304 th Hospital), Beijing 100037, China.
authors.forename: Hui-nan
authors.initials: HN
authors.lastname: Yin
authors.forename: Jia-ke
authors.initials: JK
authors.lastname: Chai
authors.forename: Yong-ming
authors.initials: YM
authors.lastname: Yao
authors.forename: Chuan-an
authors.initials: CA
authors.lastname: Shen
authors.forename: Yan-qiu
authors.initials: YQ
authors.lastname: Wu
authors.forename: Zhong-feng
authors.initials: ZF
authors.lastname: Ma
authors.forename: Qiang
authors.initials: Q
authors.lastname: Liu
authors.forename: Zhi-yong
authors.initials: ZY
authors.lastname: Sheng
mesh_terms: D006631:Amine Oxidase (Copper-Containing) / Q000097:blood; D000818:Animals; D002056:Burns / Q000150:complications / Q000503:physiopathology*; D015853:Cysteine Proteinase Inhibitors / Q000494:pharmacology; D004195:Disease Models, Animal; D007413:Intestinal Mucosa / Q000378:metabolism; D007422:Intestines / Q000503:physiopathology*; D007976:Leupeptins / Q000494:pharmacology; D008297:Male; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000378:metabolism; D046988:Proteasome Endopeptidase Complex / Q000502:physiology*; D061988:Proteasome Inhibitors; D011759:Pyrrolidines / Q000494:pharmacology; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D018805:Sepsis / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D013859:Thiocarbamates / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D025801:Ubiquitin / Q000037:antagonists & inhibitors / Q000502:physiology*
chemical_list: D015853:Cysteine Proteinase Inhibitors; D007976:Leupeptins; D016328:NF-kappa B; D061988:Proteasome Inhibitors; D011759:Pyrrolidines; D013859:Thiocarbamates; D014409:Tumor Necrosis Factor-alpha; D025801:Ubiquitin; C063261:acetylleucyl-leucyl-norleucinal; C020972:pyrrolidine dithiocarbamic acid; D006631:Amine Oxidase (Copper-Containing); D046988:Proteasome Endopeptidase Complex