Pioglitazone, a PPARγ ligand, suppresses NFκB activation through inhibition of IκB kinase activation in cerulein-treated AR42J cells

Background and aim NFκB plays a major role in the immune and inflammation responses of pancreatitis. Recently, there is increasing evidence that the expression and activity of PPARγ may participate in the activity of NFκB. Therefore, we investigated a putative relationship of the two transcription factors in cerulein-treated pancreatic acinar AR42J cells. Method AR42J were stimulated by cerulein with or without the presence of a PPARγ activator pioglitazone or a PPARγ antagonist GW9662. Results Treatment of AR42J cells with pioglitazone attenuated cerulein induced p50 and p65 NFκB dimer activity in the nucleus as measured by transcription factor assay. Cytosolic expression of IκBα protein was reduced by cerulein, basal signalling was not influenced by the PPARγ inhibitor GW9662 and pioglitazone. Adversely, the inhibitory effect of pioglitazone on NFκB activity induced by cerulein was almost reversed by GW9662. Conclusion These findings provide evidence for the involvement of the nuclear hormone receptors PPARγ in the activity of NFκB in cerulein-treated AR42J cells.