Shaoyao Gancaotang Alleviates High-fat Diet-aggravated Colitis in Mice by Suppressing Ferroptosis Through SLC7A11/GPX4 Signaling Pathway
10.13422/j.cnki.syfjx.20251906
- VernacularTitle:芍药甘草汤调控SLC7A11/GPX4信号通路抑制铁死亡缓解高脂饮食复合的小鼠结肠炎
- Author:
Juan SHI
1
;
Lianyin GAO
1
;
Xiaohui ZHANG
1
;
Jing JI
2
;
Chongyang MA
1
;
Xueqian WANG
3
;
Fafeng CHENG
3
;
Tian XU
4
Author Information
1. School of Traditional Chinese Medicine， Capital Medical University， Beijing 100069， China
2. School of Integrated Chinese and Western Medicine， Anhui University of Chinese Medicine， Hefei 230013， China
3. School of Traditional Chinese Medicine， Beijing University of Chinese Medicine， Beijing 100029， China
4. Peking Union Medical College Hospital， Chinese Academy of Medical Sciences， Beijing 100730， China
- Publication Type:Journal Article
- Keywords:
colitis;
Shaoyao Gancaotang;
high-fat diet;
ferroptosis;
transcriptomics
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2026;32(18):53-59
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the therapeutic effect of Shaoyao Gancaotang （SYGCT） on high-fat diet （HFD）-aggravated colitis induced by dextran sulfate sodium （DSS） in mice and decipher the potential mechanism. MethodsForty male C57BL/6J mice were fed an HFD for 14 days， followed by gavage of 2%DSS for 7 days for the modeling of HFD-aggravated colitis. The mice were randomly allocated into control， model （HFD-aggravated colitis）， low-dose （5.2 g·kg-1） SYGCT， high-dose （10.4 g·kg-1） SYGCT， and 5-aminosalicylic acid （5-ASA， positive control， 50 mg·kg-1） groups. Body mass changes and disease activity index （DAI） scores were recorded. The colon length was measured. Pathological changes in the colon tissue were observed through hematoxylin-eosin （HE） staining. Transcriptomic analysis was performed to identify differentially expressed genes. Western blot was employed to quantify the protein levels of Occludin， Claudin3， solute carrier family 7 member 11 （SLC7A11）， glutathione peroxidase 4 （GPX4）， and ferritin heavy chain 1 （FTH1）. ResultsCompared with the control group， the model group exhibited diarrhea， bloody stools， increased DAI scores （P<0.01）， colon shortening （P<0.01）， severe colonic pathological damage， and reduced expression of tight junction proteins Occludin and Claudin3 （P<0.05， P<0.01）. Transcriptomic analysis revealed that the differentially expressed genes between the high-dose SYGCT group and the model group were significantly enriched in the ferroptosis signaling pathway. Compared with the model group， SYGCT treatment alleviated diarrhea and bloody stools， reduced DAI scores （P<0.01）， increased the colon length （P<0.01）， mitigated colonic pathological damage， and upregulated the expression of Occludin and Claudin3 （P<0.01）， as well as proteins （SLC7A11， GPX4， and FTH1） associated with the inhibition of ferroptosis （P<0.05）. ConclusionSYGCT significantly ameliorates HFD-aggravated DSS-induced colitis by suppressing ferroptosis via activation of the SLC7A11/GPX4 pathway.
