Silibinin ameliorates Dextran Sodium Salt induced colitis in mice and prevents overexpression of inflammatory genes in lipopolysaccharide activated human macrophages

The present work was undertaken to evaluate the anti-inflammatory effect of a pure compound silibinin on Dextarn Sulfate Sodium (DSS)-induced mouse model of colitis. The expression levels of inflammatory markers such as IL-8, 5-LOX, COX-2 and iNOS in LPS activated human THP-1 derived macrophages cells were also measured. Swiss albino mice were treated with 2% DSS in their drinking water for seven days followed by one day with RO water. Silibinin (100mg and 200 mg per body weight) was administered daily through oral gavage for seven days and subsequently they were sacrificed and colon tissue samples were collected. Silibinin significantly attenuated DSS induced Disease activity Index (DAI) scores by shortening of colon length and decreased tissue Myeloperoxidase (MPO) activity that manifested as weight loss, diarrhea, rectal bleeding, and resulted in infiltrations of immune cells. Histological examination indicated that silibinin suppressed edema, mucosal damage, and the loss of crypts induced by DSS. Expression of inflammatory genes were assayed in LPS activated THP-1 derived macrophages by treating with silibinin for 24 hours when total RNA was extracted. Silibinin administration also effectively and dose dependently prevented expression of inflammatory marker genes in LPS activated THP-1 derived macrophages. These results suggest that silibinin has an anti-inflammatory effect at colorectal site suggesting its probable therapeutic role in ameliorating inflammation during colitis.