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    Effect of salidroside on Sirt1/FoxO3a slgnaling pathway induced by dextran sulfate sodium in mice with colitis

    Li Huimin;Shen Lei;Department of Gastroenterology,Renmin Hospital of Wuhan University;  
    Objective To investigate the effect of Salidroside(Sal)on Sirtl/FoxO3 a signaling pathway in dextran sulfate sodium(DSS)induced colitis mice.Methods Colitis mice model was induced by 3% DSS.Twenty-four mice were divided into control group(normal),model group(DSS),low-dose Sal group(DSS+Sal 20 mg/kg)and high-dose Sal group(DSS+Sal 40 mg/kg),with 6 mice in each group.The body weight,the activity index of colitis disease(DAI),the length of colon and the histologocal analysis were observed and recorded after 7 days.The mRNA levels of Sirtl,Fox03 a,interleukin(IL)-1,IL-6,IL-8,nuclear factor(NF)-κB p65 and tumor necrosis factor(TNF)-a in the colorectal tissue were assessed by RT-PCR.Western blotting method was used to detect the protein levels of Sirtl, FoxO3a and the phosphorylation of NF-κB p65 in coloretal tissue.Results Compared with the model group,the weight loss of mice,the scores of DAI,the colon shortening and histological damage were significantly attenuated in Sal treatment groups(P0.05 or P0.01).Sal treatment group significantly increased the expression of Sirtl and FoxO3a in colon tissue and decreased the protein level of phosphorylation of NF-κB p65(P0.05 or P0.01).The mRNA contents of IL-1,IL-6,IL-8,NF-κB p65 and TNF-a were also decreased in Sal treatment groups(P0.05 or P0.01).Conclusion Sal has a protective effect on DSS-induced colitis mice,which may be related to the Sirtl/FoxO3a pathway.
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