RGD Reference Report - Hyperbaric oxygen reduces inflammatory response in acute pancreatitis by inhibiting NF-kappaB activation. - Rat Genome Database

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Hyperbaric oxygen reduces inflammatory response in acute pancreatitis by inhibiting NF-kappaB activation.

Authors: Yu, X  Li, YG  He, XW  Li, XR  Din, BN  Gan, Y  Xu, M 
Citation: Yu X, etal., Eur Surg Res. 2009;42(2):130-5. doi: 10.1159/000196164. Epub 2009 Jan 28.
RGD ID: 10414072
Pubmed: PMID:19174608   (View Abstract at PubMed)
DOI: DOI:10.1159/000196164   (Journal Full-text)

AIM: The mechanism of hyperbaric oxygen (HBO) therapy for acute pancreatitis has not been fully clarified yet. The main purpose of this study was to investigate the effect of HBO on nuclear factor kappaB (NF-kappaB) activation and the inflammatory response in rats with acute necrotizing pancreatitis (ANP). METHODS: A total of 120 male Sprague-Dawley rats were randomly divided into 3 groups (40 in each): control, ANP and ANP + HBO. ANP rat models were established by a retrograde injection of 5% sodium taurocholate into the pancreatic duct. HBO treatment was performed at 2.5-fold absolute atmospheric pressure in 90% oxygen for 1, 3, 5, and 7 h. The activation of NF-kappaB and its inhibitor IkappaBalpha in peripheral blood neutrophilic granulocytes was measured by electrophoretic mobility shift assay and Western blot, respectively. The inflammatory cytokines [interleukin (IL)-2, IL-6, tumor necrosis factor-alpha (TNF-alpha), and intercellular adhesion molecule 1] in the blood were measured by enzyme-linked immunosorbent assay. RESULTS: The blood levels of inflammatory cytokines and NF-kappaB activation were significantly increased in ANP rats compared to control rats, but IkappaBalpha activation was suppressed. The levels of the elevated inflammatory cytokines were positively correlated with the changes in NF-kappaB activation. After HBO treatment, the blood levels of inflammatory cytokines and NF-kappaB activation were significantly decreased in the ANP + HBO group in a time-dependent manner, but IkappaBalpha activation was increased. CONCLUSION: Our findings suggest that acute pancreatitis is associated with the upregulation of cytokines in blood as well as upregulation of NF-kappaB levels and downregulation of IkappaBalpha activation in peripheral blood neutrophilic granulocytes. In contrast, HBO plays a role in acute pancreatitis treatment by normalizing these changes.



RGD Manual Disease Annotations    Click to see Annotation Detail View
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
NFKBIAHumanacute necrotizing pancreatitis treatmentISONfkbia (Rattus norvegicus) RGD 
NfkbiaRatacute necrotizing pancreatitis treatmentIEP  RGD 
NfkbiaMouseacute necrotizing pancreatitis treatmentISONfkbia (Rattus norvegicus) RGD 

Objects Annotated

Genes (Rattus norvegicus)
Nfkbia  (NFKB inhibitor alpha)

Genes (Mus musculus)
Nfkbia  (nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha)

Genes (Homo sapiens)
NFKBIA  (NFKB inhibitor alpha)


Additional Information