Betulinic acid alleviates dextran sulfate sodium-induced colitis and visceral pain in mice.

Betulinic acid (BA) exhibits many biological effects including anti-inflammatory and anti-oxidant activities. Free radicals and pro-inflammatory mediators play an important role in the pathology of inflammatory bowel disease (IBD) and associated pain. We, therefore, examined the anti-oxidant, anti-inflammatory, and anti-nociceptive potential of BA in colitis. Colitis was induced with 3% (w/v) dextran sulfate sodium (DSS) in drinking water in mice for 1to7 days. BA (3, 10 and 30 mg/kg) was given orally for 0 to 7 days. BA was also tested for its efficacy in acetic acid and mustard oil-induced visceral nociception in mice at same doses. BA significantly prevented diarrhea; bleeding and colonic pathological changes induced by DSS. Further, BA reduced the colon nitrite, malondialdehyde, myeloperoxidase, and lipid hydroperoxide levels and restored the superoxide dismutase, catalase and reduced glutathione levels to normalize the redox balance in DSS-exposed mice. Inflammatory mediators like matrix metalloproteinase-9 and prostaglandin E2 levels were also significantly attenuated by BA in colitis mice. Additionally, BA reduced acetic acid and mustard oil-induced visceral pain in mice. In conclusion, the results of the present study suggest that BA possesses good anti-nociceptive activity and the anti-IBD effects of BA are due to its anti-oxidant and anti-inflammatory potential.