中国免疫学杂志2024，Vol.40Issue(7)：1461-1466,6.DOI:10.3969/j.issn.1000-484X.2024.07.019
冬凌草甲素介导Sirt1信号轴抑制溃疡性结肠炎的机制研究
Mechanism study on inhibition of ulcerative colitis by Sirt1 signaling axis mediated by oridonin
摘要
Abstract
Objective:To build mice ulcerative colitis(UC)model by dextran sodium sulfate salt(DSS),and to explore effect and molecular mechanism of oridonin(Ori)on alleviating UC by mediating Sirt1 signaling pathway,as well as to find new drugs for UC treatment.Methods:Sixty BALB/c mice were randomly divided into normal group(NC),model group(DSS),DSS+mesalazine sustained-release granule group(AC),DSS+low-dose Ori group(Ori-L),DSS+medium-dose Ori group(Ori-M)and DSS+high-dose Ori group(Ori-H),with 10 mice in each group.Except NC group,mice in other groups were given 3%DSS aqueous solution free for 7 days.After successful modeling,Ori-L group,Ori-M group and Ori-H group were intragastric with 50,100 and 150 mg/kg Ori suspension,respectively.NC group and DSS group drank distilled water free,AC group was intragastric with mesalazine sustained-release granules 100 mg/kg,lasted for 10 days.Weight changes of mice were recorded and disease active index(DAI)score was performed.After treatment,serum levels of IL-1β and tumor necrosis factor-α(TNF-α)were detected by ELISA.Whole colon tissues were extracted,length was measured,and HE staining was performed.Real-time fluorescence quantitative PCR and Western blot were used to detect expressions of Sirt1,NF-κB and p53 in colon tissues of each group.Results:After successful modeling,compared with NC group,the other 5 groups of mice showed weight loss,DAI score increased and colon length shortened,Sirt1 expression was signi-ficantly inhibited,while expressions of NF-κB and p53 were significantly increased,accompanied by obvious inflammatory pathologi-cal features.Compared with DSS group,Ori-L,Ori-M,and Ori-H groups and AC group had less weight loss during experiment,and DAI scores showed lower disease activity and relatively less colon length shortening,Sirt1 expression was less inhibited,expressions of NF-κB and p53 were also relatively small.Results of AC group could prove that Ori has therapeutic effect on UC.Conclusion:Ori can improve UC in mice,whose effect may be related to regulation of Sirt1 signal.关键词
冬凌草甲素/溃疡性结肠炎/Sirt1信号通路/炎症因子Key words
Oridonin/Ulcerative colitis/Sirt1 signaling pathway/Inflammation factors分类
医药卫生引用本文复制引用
王茂楠,徐博,李林玥,李姝蓉,李明成..冬凌草甲素介导Sirt1信号轴抑制溃疡性结肠炎的机制研究[J].中国免疫学杂志,2024,40(7):1461-1466,6.基金项目
吉林省科技厅自然科学基金(YDZJ202301ZYTS122). （YDZJ202301ZYTS122）
