Huangqi Baijiang Yiren Decoction Restores Intestinal Mucosa Barrier in Rat Model of Ulcerative Colitis via miR-21/SOCS1/JAK1/STAT6 Signaling Pathway
10.13422/j.cnki.syfjx.20242440
- VernacularTitle:基于miR-21/SOCS1/JAK1/STAT6信号通路探讨黄芪败酱薏仁汤对溃疡性结肠炎大鼠肠黏膜屏障的修复作用
- Author:
Ruiping LI
1
;
Shiyu WANG
1
;
Xiunan WEI
1
;
Ermei WU
1
;
Dajuan SUN
2
Author Information
1. The First Clinical Medical College of Shandong University of Traditional Chinese Medicine（TCM）， Jinan 250014， China
2. Affiliated Hospital of Shandong University of TCM，Jinan 250014， China
- Publication Type:Journal Article
- Keywords:
ulcerative colitis;
Huangqi Baijiang Yiren decoction;
miR-21/suppressor of cytokine signaling 1 （SOCS1）/Janus kinase 1 （JAK1）/signal transducer and activator of transcription 6 （STAT6） signaling pathway;
intestinal mucosa barrier
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2025;31(16):96-104
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo explore the potential mechanism by which Huangqi Baijiang Yiren decoction （HBY） repairs the intestinal mucosal injury in the rat model of ulcerative colitis （UC） via the miR-21/suppressor of cytokine signaling 1 （SOCS1）/Janus kinase 1 （JAK1）/signal transducer and activator of transcription 6 （STAT6） signaling pathway. MethodsSixty SPF-grade male SD rats were randomly assigned into six groups： blank， model， low-dose （3.68 g·kg-1） HBY， medium-dose （7.35 g·kg-1） HBY， high-dose （14.5 g·kg-1） HBY， and mesalazine （0.035 g·kg-1）， with 10 rats in each group. The rat model of UC was established in other groups except the blank group by 3% dextran sulfate sodium solution. The rats were administrated with corresponding drugs once a day for 7 consecutive days since the 3th day after modeling. The histopathological changes of the colon were observed by hematoxylin-eosin staining， and the Robarts histopathology index （RHI） was scored. Enzyme-linked immunosorbent assay was employed to measure the levels of pro-inflammatory cytokines ［interleukin （IL）-6， IL-18， IL-1β， and tumor necrosis factor-α （TNF-α）］ in the serum. Real-time PCR was employed to determine the mRNA levels of miR-21， SOCS1， JAK1， and STAT6 in the colon tissue. Western blot was employed to determine the protein levels of SOCS1， JAK1， phosphorylated （p）-JAK1， STAT6， p-STAT6， Occludin， and Claudin-1 in the colon tissue. ResultsCompared with the blank group， the model group showed an increase in disease activity index （DAI） （P<0.01）， shortening of colon length （P<0.01）， severe histopathological damage in the colon tissue， and an increase in RHI， rises in serum levels of IL-6， IL-1β， IL-18， and TNF-α （P<0.01）， up-regulation in mRNA levels of miR-21， JAK1， and STAT6 and protein levels of p-JAK1 and p-STAT6 （P<0.01）， and down-regulation in mRNA and protein levels of SOCS1 and protein levels of Occludin and Claudin-1 （P<0.01）. The treatment with HBY reduced the DAI （P<0.01）， alleviated colon shortening and histopathological damage in the colon tissue， decreased the RHI （P<0.01）， lowered the serum levels of IL-6， IL-1β， IL-18， and TNF-α （P<0.01）， down-regulated the mRNA levels of miR-21， JAK1， and STAT6 （P<0.05， P<0.01）， up-regulated the mRNA level of SOCS1 （P<0.05）， up-regulated the protein levels of SOCS1， Occludin， and Claudin-1 （P<0.05， P<0.01）， and down-regulated the protein levels of p-JAK1 and p-STAT6 （P<0.05， P<0.01）. ConclusionHBY may modulate the miR-21/SOCS1/JAK1/STAT6 signaling pathway to suppress inflammatory responses and restore the intestinal mucosal barrier in UC rats.
