scholarly journals PPAR-αContributes to the Anti-Inflammatory Activity of Verbascoside in a Model of Inflammatory Bowel Disease in Mice

PPAR Research ◽  
2010 ◽  
Vol 2010 ◽  
pp. 1-10 ◽  
Author(s):  
Emanuela Esposito ◽  
Emanuela Mazzon ◽  
Irene Paterniti ◽  
Roberto Dal Toso ◽  
Giovanna Pressi ◽  
...  

The previous results suggest that peroxisome proliferator-activated receptor-alpha (PPAR)-α, an intracellular transcription factor activated by fatty acids, plays a role in control of inflammation. There is persuasive epidemiological and experimental evidence that dietary polyphenols have anti-inflammatory activity. In this regard, it has been demonstrated that verbascoside (VB) functions as intracellular radical scavenger and reduces the microscopic and macroscopic signs of experimental colitis. With the aim to characterize the role of PPAR-αin VB-mediated anti-inflammatory activity, we tested the efficacy of VB in an experimental model of inflammatory bowel disease induced by dinitrobenzene sulfonic acid, comparing mice lacking PPAR-α(PPAR-αKO) with wild type (WT) mice. Results indicate that VB-mediated anti-inflammatory activity is weakened in PPAR-αKO mice, compared to WT controls, especially in the inhibition of neutrophil infiltration, intestinal permeability and colon injury. These results indicate that PPAR-αcan contribute to the anti-inflammatory activity of VB in inflammatory bowel disease.

PPAR Research ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Vito Annese ◽  
Francesca Rogai ◽  
Alessia Settesoldi ◽  
Siro Bagnoli

Peroxisome proliferator-activated receptor gamma (PPARγ) is member of a family of nuclear receptors that interacts with nuclear proteins acting as coactivators and corepressors. The colon is a major tissue which expresses PPARγin epithelial cells and, to a lesser degree, in macrophages and lymphocytes and plays a role in the regulation of intestinal inflammation. Indeed, both natural and synthetic PPARγligands have beneficial effects in different models of experimental colitis, with possible implication in the therapy of inflammatory bowel disease (IBD). This paper will specifically focus on potential role of PPARγin the predisposition and physiopathology of IBD and will analyze its possible role in medical therapy.


2008 ◽  
Vol 115 (4) ◽  
pp. 107-127 ◽  
Author(s):  
Jeffrey M. Peters ◽  
Holly E. Hollingshead ◽  
Frank J. Gonzalez

PPARβ/δ (peroxisome-proliferator-activated receptor β/δ) is one of three PPARs in the nuclear hormone receptor superfamily that are collectively involved in the control of lipid homoeostasis among other functions. PPARβ/δ not only acts as a ligand-activated transcription factor, but also affects signal transduction by interacting with other transcription factors such as NF-κB (nuclear factor κB). Constitutive expression of PPARβ/δ in the gastrointestinal tract is very high compared with other tissues and its potential physiological roles in this tissue include homoeostatic regulation of intestinal cell proliferation/differentiation and modulation of inflammation associated with inflammatory bowel disease and colon cancer. Analysis of mouse epithelial cells in the intestine and colon has clearly demonstrated that ligand activation of PPARβ/δ induces terminal differentiation. The PPARβ/δ target genes mediating this effect are currently unknown. Emerging evidence suggests that PPARβ/δ can suppress inflammatory bowel disease through PPARβ/δ-dependent and ligand-independent down-regulation of inflammatory signalling. However, the role of PPARβ/δ in colon carcinogenesis remains controversial, as conflicting evidence suggests that ligand activation of PPARβ/δ can either potentiate or attenuate this disease. In the present review, we summarize the role of PPARβ/δ in gastrointestinal physiology and disease with an emphasis on findings in experimental models using both high-affinity ligands and null-mouse models.


2012 ◽  
Vol 18 (3) ◽  
pp. 472-479 ◽  
Author(s):  
Szilard Poliska ◽  
Andras Penyige ◽  
Peter Laszlo Lakatos ◽  
Maria Papp ◽  
Karoly Palatka ◽  
...  

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