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P035. Salicin ameliorates the inflammation and prevents the loss of gut flora in DSS induced mice model of colitis

N.V. Nirmal Verma1, J.P. Jaishree Paul2, 1Jawaharlal Nehru University, School of Life Sciences, New Delhi, India, 2Jawahrlal Nehru University, School of Life Sciences, New Delhi, India


Crohn's disease (CD) and ulcerative colitis (UC) are two related but distinct chronic inflammatory disorders of the gastrointestinal tract, commonly denoted as inflammatory bowel diseases (IBD). Preliminary research suggests that people with inflammatory bowel disease especially those with ulcerative colitis may be at increased risk for developing colorectal cancer and pancreatic cancer. Other studies have shown that people with IBD are five times more likely to develop colon cancer compared to non IBD patients. In order to study etiology of IBD, mouse experimental colitis induced by oral administration of Dextran sulfate sodium (DSS) is widely used as a standardized colitis model. Willow bark (Salix species) has been used throughout the world for centuries as an anti-pyretic and analgesic agent. Its active constituents, Salicin, and its derivates were widely used by 19th century physicians to treat rheumatic fever, different kinds of pain, including back pain, toothache, and headache. The present work was undertaken to evaluate the anti-inflammatory effect of Salicin and its role in preventing loss of gut flora on DSS treated mice.


Experimental colitis was induced in Swiss albino mice by dissolving 2% DSS in their drinking water for 7 days. Salicin (100 mg and 200 mg per body weight) was administered daily intraperitonialy for 7 days. Genomic DNA was isolated at regular intervals from fresh stool of mice and gut flora were quantified by Real time PCR.


Salicin significantly attenuated DSS induced Disease activity Index (DAI) scores and tissue Myleoperoxidase (MPO) activity, which implied that it suppressed weight loss, diarrhea, gross bleeding, and the infiltrations of Immune cells. Salicin administration also effectively and dose dependently prevented shortening of colon length in DSS induced colitis mouse. Histological examination indicated anti-inflammatory effect of Salicin as it suppressed edema, mucosal damage, and the loss of crypts induced by DSS. Furthermore, prevention in the loss of selected gut flora (Lactobacillus, Bifidobacteria, Bacteroides, Ruminococcus and Methanobrevibacter) were also observed till two days of salicin treatment.


These results suggest that Salicin has an anti-inflammatory effect at colorectal site, and it may have therapeutic value in ameliorating inflammation during IBD.