Peroxisome proliferator-activated receptor-gamma (PPAR-γ) expression is downregulated in patients with active ulcerative colitis

Abstract

FIGURE 1. Gene expression of PPAR-c in rectal mucosa from patients with UC (active/remission) and the constitutive gene RPL0.

Peroxisome proliferator-activated receptor-γ is downregulated in ulcerative colitis and is involved in experimental colitis-associated neoplasia

“…These findings demonstrated that deregulation of PPAR-γ may play an important role in the pathogenic process of UC. The present data were also consistent with the results obtained by Yamamoto-Furusho et al (25), which indicated that the mRNA expression of PPAR-γ was decreased in rectal mucosa from patients with active UC compared with UC patients in remission, and PPAR-γ gene expression was negatively correlated with endoscopic activity, as determined by Spearman correlation test. The present study did not identify a correlation between the expression of PPAR-γ and the site of UC lesions, which indicates that PPAR-γ was involved in an alternative component of the UC intestinal inflammation.…”

Prophylactic effects of triptolide on colon cancer development in azoxymethane/dextran sulfate sodiuminduced mouse model

“…The levels of both metalloproteinase-2 and metalloproteinase-9 were markedly increased after incubation of HCT116 cells with triptolide. A previous study demonstrated that active PPARγ caused the inhibition of alimentary canal inflammation; thus, its expression is of significance for the treatment of colon cancer [26]. Our study demonstrated that triptolide treatment of AOM/DSS mice significantly prevented colon tissue inflammation.…”

PPARγ ligand attenuates portal inflammation in the MRL-lpr mouse: a new strategy to restrain cholangiopathy in primary biliary cirrhosis

“…12 In addition to the biliary epithelial cells of PBC, a reduction of PPARγ expression in the colonic epithelial mucosa is reportedly associated with the pathogenesis of inflammatory bowel diseases (IBD). [13][14][15][16] Furthermore, the expression of PPARγ is affected by the commensal intestinal flora and ligands (agonists) for PPARγ can attenuate colitis in IBD-model mice, supporting the notion that PPARγ ligands may have salutary effects on IBD. 14,[16][17][18] As for anti-inflammatory activities, the activation of PPARγ by its ligands is shown to inhibit the expression of pro-inflammatory cytokines, the induction of which is mediated via NF-κB and mitogen activated protein kinase (MAPK).…”