Quercetin and chlorogenic acid affect butyrate excretion, NF‐ κB activity, and cell proliferation in DSS treated rats

We previously showed quercetin was protective against colon carcinogenesis via inhibition of pro‐inflammatory molecules. The goal of this study was to explore effects of quercetin and chlorogenic acid (CA), stone fruit bioactives, on short chain fatty acid (SCFA) excretion and cell proliferation regulation in a colitis/injury model. Rats (n=63) received diets (basal, 0.05% CA, or 0.45% quercetin) for 3 wk before dextran sodium sulfate (DSS, 3%, 3x, 2 wk separation, n=11/diet) or control (no DSS, n=10/diet) treatments. SCFA concentration and fecal moisture were measured in feces collected pre‐ and post‐DSS treatments and on day 62. Colons were assessed for injury, inflammation, and proliferative index (PI), and mucosal scrapings for NF‐κB activity. DSS increased fecal moisture by 38.7% and SCFA concentration by 139.6% (p<0.0001). Quercetin, a butyrate uptake inhibitor, tended to increase 24 h butyrate excretion in DSS rats relative to basal (p=0.07) and CA (p=0.09). Quercetin and CA diets increased NF‐κB activity and PI (p<0.05) in control rats. Compared to non‐DSS rats, CA decreased NF‐κB activity and PI in DSS rats (p<0.05). Although quercetin and CA affected butyrate excretion, NF‐κB activity, and proliferation, and had no effect on injury, it may be possible these compounds would mitigate injury if given a longer recovery period. Funded by USDA/NIFA 2008‐34402‐19195 and 2009‐34402‐19195.