ABSTRACT
Quercitrin, 3-rhamnosylquercetin, is a bioflavonoid with antioxidant properties, which exerts anti-inflammatory activity in experimental colitis. In the present study, different in vivo experiments were performed in order to evaluate the mechanisms of action involved in this effect, with special attention to its effects on proinflammatory mediators, including nitric oxide (NO). Experimental colitis was induced in female Wistar rats by incorporation of dextran sodium sulfate (DSS) in drinking water. Oral treatment of quercitrin (1 or 5 mg kg(-1) day(-1)) to colitic rats ameliorated the evolution of the inflammatory process induced when administered in a preventative dosing protocol. When quercitrin (1 mg kg(-1) day(-1)) was administered on established colitis, it facilitated the recovery of the inflamed mucosa. The beneficial effects exerted by quercitrin were evidenced both histologically and biochemically, and were associated with an improvement in the colonic oxidative status, altered as a consequence of the colonic insult induced by DSS. In addition, a reduction of colonic NO synthase activity was observed, probably related to a decreased expression in the inducible form of the enzyme via downregulation in the colonic activity of the nuclear factor-kappaB. Immunohistochemical studies showed that quercitrin treatment reduced macrophage and granulocyte infiltration in the inflamed tissue.
