湖南中医药大学学报2025，Vol.45Issue(3)：417-424,8.DOI:10.3969/j.issn.1674-070X.2025.03.004
复方芩柏颗粒通过调控Claudin-1表达及JAK2/STAT3信号通路缓解小鼠溃疡性结肠炎
Compound Qinbai Granule relieving ulcerative colitis in mice by regulating Claudin-1 expression and JAK2/STAT3 signaling pathway
摘要
Abstract
Objective To explore the mechanism of action of Compound Qinbai Granule(CQBG)in treating ulcerative colitis(UC)and to study its regulatory effects on inflammatory response,oxidative stress,intestinal mucosal barrier function,and Janus kinase 2(JAK2)/signal transducer and activator of transcription 3(STAT3)signaling pathway.Methods The UC model of C57B/L mice was established by 2,4,6-trinitrobenzenesulfonic acid/ethanol enema method and the mice were randomly divided into normal control,UC model,inhibitor,olsalazine,and CQBG groups.Mice in the normal control group received an enema of saline of equal volume.Each group consisted of six mice.The pathological damage of colon tissue was observed by HE staining,the protein expression level of Claudin-1 was determined by immunohistochemical staining,and the levels of oxidative stress-related factors such as superoxide dismutase(SOD),catalase(CAT),and malondialdehyde(MDA),as well as inflammatory factors including tumor necrosis factor-α(TNF-α),interleukin(IL)-6,IL-10,IL-12,and transforming growth factor-β(TGF-β),were measured by ELISA.The mRNA and protein expression of Claudin-1,JAK2,and STAT3 were determined by RT-qPCR and Western blot,respectively.Results Compared with the normal control group,the CMDI and DAI scores,the levels of MDA,TNF-α,IL-6,and IL-12,the relative expression levels of JAK2 and STAT3 mRNA,and the protein expression levels of p-JAK2/JAK2 and p-STAT3/STAT3 in the UC model group increased(P<0.05),while the SOD activity,the levels of CAT,GSH,IL-10,TGF-β,and IL-4,the protein and mRNA expression levels of Claudin-1,and the protein expression level of Claudin-1 in the UC model group decreased(P<0.05).Compared with the UC model group,the CMDI and DAI scores,the levels of MDA,TNF-α,IL-6,and IL-12,the relative expressions of JAK2 and STAT3 mRNA,and the protein expressions of p-JAK2/JAK2 and p-STAT3/STAT3 in the inhibitor,olsalazine,and CQBG groups decreased(P<0.05),while the SOD activity,the levels of CAT,GSH,IL-10,TGF-β,and IL-4,and the protein and mRNA expression levels of Claudin-1 increased(P<0.05).Conclusion CQBG can treat UC by regulating oxidative stress,inflammatory response and intestinal barrier function,and inhibiting the activation of JAK2/STAT3 signaling pathway.关键词
溃疡性结肠炎/JAK2/STAT3信号通路/氧化应激/炎症/肠道黏膜屏障功能Key words
ulcerative colitis/Janus kinase 2/signal transducer and activator of transcription 3 signaling pathway/oxida-tive stress/inflammation/intestinal mucosal barrier function分类
医药卫生引用本文复制引用
王晓燕,肖超,王真权,肖佑..复方芩柏颗粒通过调控Claudin-1表达及JAK2/STAT3信号通路缓解小鼠溃疡性结肠炎[J].湖南中医药大学学报,2025,45(3):417-424,8.基金项目
湖南省中医药管理局课题(B2023095,C2024017) （B2023095,C2024017）
湖南中医药大学校级课题(2022XYLH031). （2022XYLH031）
