Effect of Hongyuyin inhibiting oxidative stress on inflammatory bowel disease induced by dextran sodium sulfate in mice based on Nrf2/HO-1 signaling pathway
Objective To explore the protective effect of Hongyuyin inhibiting oxidative stress on inflammatory bowel disease in-duced by dextran sodium sulfate in mice based on Nrf2/HO-1 signaling pathway.Methods Fifty mice were randomly divided in-to normal group,model group and low,medium and high dosage groups of Hongyuyin(8.95,17.89 and 35.76g/kg),with 10 mice in each group.Establish models for other groups except for the normal group.Inflammatory bowel disease(IBD)model was established by drinking 2.5％DSS freely.Hongyuyin group was given low,medium and high doses of Hongyuyin by gavage re-spectively,and normal group and model group were given equal volume of normal saline by gavage for 7 days.The body weight,feces and mental state of mice were recorded every day,and the disease activity index(DAI)was scored.On the 14th day,all mice were killed,the length of colorectal cancer was recorded,and histopathological changes were observed by HE staining.The level of CAT and GSH-Px in colon tissue was detected by biochemical kit.The protein and mRNA expressions of Nrf2、HO-1 in colon tissue were detected by Western blot and Quantitative Real-time PCR.Results Compared with the normal group,DAI score,colonic histopathology score,of the model group were increased(P＜0.01),the level of CAT and GSH-Px and the ex-pression of Nrf2、HO-1 protein and mRNA were all decreased(P＜0.01),the colon length was shortened(P＜0.01),and the intestinal wall tissue was damaged.Compared with the model group,the DAI score,colonic histopathology score were all de-creased in each dosage group of Hongyuyin,the length of colon and the level of CAT and GSH-Px and the expressions of Nrf2、HO-1 protein and mRNA were all increased(P＜0.01),and the damage of intestinal wall tissue was improved.Conclusion Hongyuyin can regulate Nrf2/HO-1 signaling pathway by inhibiting oxidative stress to treat IBD induced by DSS in mice.
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