The therapeutic effects and mechanism of isoorientin on dextran sodium sulfate-induced ulcerative colitis in mice
Objective:To study the protective effects of isoorientin(ISO)against chronic ulcerative colitis(UC)induced by dextran sulfate sodium(DSS)in mice.Methods:Forty C57BL/6 mice were randomly divided into five groups:control group,DSS group(2%DSS),mesalazine(5-ASA,150 mg·kg-1·d-1)+ DSS group,low-dose ISO(L-ISO,10 mg·kg-1·d-1)+ DSS group,and high-dose ISO(H-ISO,20 mg·kg-1·d-1)+ DSS group,with 8 mice in each group.The mice were treated by ISO gavage for 37 days before they were executed by spinal dislocation.The colonic tissues were collected and their lengths were recorded.The levels of inflammatory cytokines in the colon tissues were measured by ELISA.The histopathological changes of mice colon tissues were observed by HE staining,and the mucin secretion levels of mice colon tissues were observed by AB-PAS staining.Ultrastructure of colonic mucosa was observed by transmission electron microscope.The expression levels of P-glycoprotein were analyzed by Western Blot.Results:Compared with the DSS group,ISO significantly alleviated body weight loss(P<0.01),colon length shortening(P<0.05),disease activity index(DAI)scores(P<0.05),histopathological score(P<0.05),and the decrease of mucin(P<0.01)in mice with DSS-induced colitis.The levels of TNF-α(P<0.01)and IL-6(P<0.05)in colonic tissues decreased significantly in mice treated with ISO.Further,ISO administration repaired the damaged intestinal mucosal barrier and upregulated the expression level of P-glycoprotein(P<0.05)in colon tissues.Conclusion:Isoorientin has protective effects on chronic ulcerative colitis induced by DSS in mice.The mechanism may be attributed to its repairing effect on the intestinal mucosal barrier damage and modulating function to the expression of P-glycoprotein in colitis tissues.
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万方数据
维普
