Evaluation of the inhibitory potential of flavonoid-rich fraction of Myrica esculenta against DSS-induced colonic inflammation in mice

Abstract

Abstract Background Myrica esculenta (family Myricaceae) is a plant species valued in India and China for the management of gut disorders. Scientific validation of its anti-ulcerative colitis activity was aimed. Methods and Results The ethyl acetate fraction of Myrica esculenta (MeEa) was prepared and evaluated for its potency against DSS-induced ulcerative colitis (UC) in mice at 200 and 400 mg/kg BW oral dose. The effective dose of MeEa was determined through its effect on DSS-induced UC and was further analyzed through its effects on disease activity index (DAI), colon length, colon weight/length ratio, spleen weight, serum and colon tissue cytokine level, cell count (total WBC, lymphocytes, monocytes, granulocytes, RBC and platelet) and hemoglobin content. Furthermore, the effect was determined through histopathology and FITC-dextran-induced membrane permeability assay. Between the two doses MeEa at 400 mg/kg BW was found to be the most effective dose in terms of reduced DAI scores, which were increased due to DSS administration, protected colon length from shortening, decreased colon weight/length ratio, reduced spleen weight, decreased pro-inflammatory cytokine (IL6, IL8, TNF α and IFN γ) level and stabilized the anti-inflammatory cytokine (IL10) level in serum and colon tissue. MeEa 400 reduced cell counts and increased hemoglobin content and platelet count. Furthermore, MeEa 400 prevented the colon by protecting epithelial cells and crypts. MeEa 400 provided significant protection from intestinal leakage and reduced FITC dextran level in serum. Conclusions MeEa 400 possesses significant anti-inflammatory potential and acts via attenuation of DSS-induced UC and inhibition of DAI scores. It reduces pro-inflammatory cytokines and stabilizes anti-inflammatory cytokine levels, reduces cell count, and protects epithelial tissue and crypts in the colon as well as intestinal membrane leakage that occurred due to FITC-dextran administration in mice.