RGD Reference Report - Cell-permeable Tat-NBD peptide attenuates rat pancreatitis and acinus cell inflammation response. - Rat Genome Database

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Cell-permeable Tat-NBD peptide attenuates rat pancreatitis and acinus cell inflammation response.

Authors: Long, You-Ming  Chen, Ken  Liu, Xue-Jin  Xie, Wen-Rui  Wang, Hui 
Citation: Long YM, etal., World J Gastroenterol. 2009 Feb 7;15(5):561-9.
RGD ID: 12791282
Pubmed: PMID:19195057   (View Abstract at PubMed)
PMCID: PMC2653342   (View Article at PubMed Central)


AIM: To investigate the effects of Tat-NEMO-binding domain (NBD) peptide on taurocholate-induced pancreatitis and lipopolysaccharide (LPS)-stimulated AR42J acinus cells inflammatory response in rats.
METHODS: Sodium taurocholate (5%) was used to induce the pancreatitis model. Forty-eight rats from the taurocholate group received an intravenous bolus of 13 mg/kg Tat-NBD (wild-type, WT) peptide, Tat-NBD (mutant-type, MT) peptide, NBD peptide or Tat peptide. The pancreatic histopathology was analyzed by hematoxylin staining. LPS was added to the culture medium to stimulate the AR42J cells. For pretreatment, cells were incubated with different peptides for 2 h before LPS stimulation. Expression of IL-1beta and TNF-alpha mRNA was analyzed using a semi-quantitative reverse-transcript polymerase chain reaction (RT-PCR) method. IL-1beta and TNF-alpha protein in culture medium were detected by enzyme linked immunosorbent assay (ELISA). NF-kappaB DNA-binding in pancreas was examined by electrophoretic mobility shift assays. P65 expression of AR42J was determined by Strept Actividin-Biotin Complex (SABC) method.
RESULTS: Pretreatment with Tat-NBD (WT) peptide at a concentration of 13 mg/kg body wt showed beneficial effect in pancreaitis model. LPS (10 mg/L) resulted in an increase of IL-1beta mRNA, IL-1beta protein, TNF-alpha mRNA and TNF-alpha protein, whereas significantly inhibitory effects were observed when cells were incubated with Tat-NBD (WT). Consisting with p65 expression decrease analyzed by SABC method, NF-kappaB DNA-binding activity significantly decreased in Tat-NBD (WT) pretreatment group, especially at the largest dose. No significant changes were found in the control peptide group.
CONCLUSION: Our result supports that active NF-kappaB participates in the pathogenesis of STC-induced acute pancreatitis in rats. Tat-NBD (WT) peptide has anti-inflammatory effects in this model and inhibits the inflammation of acinus simulated by LPS.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Experimental Pancreatitis treatmentISOIkbkg (Rattus norvegicus)12791282; 12791282 RGD 
Experimental Pancreatitis treatmentIDA 12791282 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Ikbkg  (inhibitor of nuclear factor kappa B kinase regulatory subunit gamma)

Genes (Mus musculus)
Ikbkg  (inhibitor of kappaB kinase gamma)

Genes (Homo sapiens)
IKBKG  (inhibitor of nuclear factor kappa B kinase regulatory subunit gamma)


Additional Information