Introduction
Inflammatory bowel disease (IBD) represents a cluster of chronic systemic intestinal disturbances that comprise Crohn’s disease (CD) and ulcerative colitis. It has been shown that the transcription factor peroxisome proliferator activated receptor-gamma (PPAR-α) exerts its anti-inflammatory action by negatively influencing the expression and activity of inflammatory transcription factor called NF-kb. In the absence of (PPAR-α) gene, IBD pathologies are exacerbated. (1) We have previously shown that the polyphenolic extract from maqui fruit decreased reactive oxygen species (ROS) in a dose-dependent manner and its administration in an experimental animal model of CD significatively ameliorated the clinical course of the disease and intestinal inflammation.
Aims & Methods
We explored whether maqui extract had an anti-inflammatory role through modulating PPAR-α expression in epithelial cells and macrophage cells from colon tissue. Male Balb/c mice 12-14 weeks old which were exposed to 2,4,6-trinitrobenzene sulfonic acid (TNBS) via intracolonic administration and were randomly assigned in 4 groups (n=6) as follows: i) Control Group (EtOH 50%) ii) Crohn’s Disease Group (100 mg/kg of TNBS plus EtOH 50%), iii) Curative Group (maqui at 50mg/kg for 4 days after TNBS induction), iv) Preventive Group (maqui at 50mg/kg 7 days prior TNBS and 4 days after induction).
Results
In the epithelial cells, TNBS induced a slight decrease of PPAR-α expression when we compared with the control group. Notably, this difference did not reach statistical significance. The administration of maqui extract did not alter epithelial PPAR-α level. Similar PPAR-α staining intensity and expression was showed either for curative or preventive groups remained like the control group.
In terms of specific macrophage PPAR-α levels, a stronger positive staining and intensity was observed in the CD mice when compared to the controls. However, this difference was not significant. Similarly, an increase in PPAR-α staining intensity and PPAR-α positive macrophages was also observed in mice that received curative maqui treatment, whereas colons from mice receiving maqui extract as a preventive treatment yielded a significative PPAR-α staining.
Conclusion
Maqui extract treatment elicit an anti-inflammatory action by increasing the expression of PPAR-α in immune cells during the earlier phase of the disease. These data support the preventive effect of polyphenols from maqui extract and its potential antiinflammatory effect in IBD.
References
1. Leng F, Yin H, Qin S, Zhang K, Guan Y, Fang R, et al. NLRP6 self-assembles into a linear molecular platform following LPS binding and ATP stimulation. Sci Rep. 2020;10(1):1–10.