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AIM: To investigate the potential of atractylenolide Ⅲ(AⅢ) in mitigating dextran sulfate sodium (DSS)-induced injury in a mouse model of chronic inflammatory bowel disease (IBD), and to explore the mechanisms involved, particularly the modulation of signal transducer and activator of transcription 3 (STAT3) signaling, which plays a crucial role in the homeostasis of T helper 17(Th17) and regulatory T(Treg) cells. METHODS: A mouse model of DSSinduced chronic IBD was established, and the mice were divided into 4 groups: control, model(DSS), high-dose(50 mg/kg) AⅢ, and low-dose (30 mg/kg) AⅢ. The disease activity index (DAI) was utilized to assess disease severity. Histopathological damage in the colons of IBD mice was evaluated by hematoxylin-eosin (HE) staining. The protein levels of phosphorylated STAT3, occludin and zonula occludens-1 (ZO-1) were analyzed using immunohistochemical staining and Western blot. Flow cytometry was employed to examine the differentiation of splenic lymphocytes into Th17/Treg cells. RESULTS: Both DAI assessments and HE staining indicated that AⅢ significantly alleviated inflammatory injury in mice with DSS-induced chronic IBD. Immunohistochemical analysis demonstrated that AⅢ enhanced the expression of ZO-1 and occludin in colonic tissues. Flow cytometry results revealed that AⅢ helped maintain the balance between splenic Th17 and Treg cells. Furthermore, immunohistochemical staining and Western blot showed that AⅢ inhibited the phosphorylation of STAT3. CONCLUSION: Treatment with AⅢ effectively reduced inflammatory injury in a mouse model of chronic IBD by preserving Th17/Treg homeostasis through the inhibition of STAT3 phosphorylation. As a natural compound, AⅢ exhibits significant therapeutic potential for the treatment of chronic IBD. [ABSTRACT FROM AUTHOR]

AIM: To explore the effect and mechanism of action of the aqueous extract of Fritillaria ussuriensis （FU-AE） against nonalcoholic fatty liver disease （NAFLD）. METHODS: The association between Fritillaria ussuriensis Maxir.（ FU） and NAFLD was analyzed by network pharmacology. A mouse model of NAFLD was induced in mice by high fat diet （HFD） + 10% fructose drinking water, and three doses of Fritillaria ussuriensis aqueous extract were given to the mice for intervention. Colorimetric assay was used for detection of aspartate aminotransferase （AST）, alanine aminotransferase （ALT）, triglyceride （TG）, total cholesterol （TC）, high-density lipoprotein cholesterol （HDL-C）, and low-density lipoprotein cholesterol （LDL-C） levels in the serum of experimental mice. Hematoxylin and eosin staining was used to assess the pathological and histological changes in the liver of mice and to clarify the anti-NAFLD effect of aqueous extracts of Fritillaria ussuriensis. Liver tissue proteins were extracted, and expression of proteins related to the AMP-activated protein kinase（ AMPK）/acetyl-CoA carboxylase（ ACC） pathway was detected by Western blot to clarify the mechanism of anti-NAFLD action of Fritillaria ussuriensis. The microbial composition of cecum contents was explored using 16S rRNA sequencing to reveal the modulatory effect of the aqueous extract of Fritillaria ussuriensis on the structure of intestinal flora in mice with nonalcoholic fatty liver disease. RESULTS: Aqueous extract of Fritillaria ussuriensis （high dose） ameliorated exogenous adipocyte infiltration in the liver of mice with NAFLD （P<0. 05）. AST, ALT, TG, TC and LDL-C levels were significantly decreased（ P<0. 05） and HDL-C levels were significantly increased（ P<0. 05） in the high-dose group. Aqueous extract of Fritillaria ussuriensis （high dose） significantly increased expression of phosphorylated AMPKα, AMPKα, and phosphorylated ACC in the livers of the model mice （P<0. 05）, significantly reduced expression of ACC （P<0. 05）, and significantly increased the relative abundance of the potentially beneficial bacteria Faecalibaculum rodentium, Lactobacillus johnsonii, Akkermansia muciniphila （P<0. 05）. CONCLUSION: Aqueous extract of Fritillaria ussuriensis may ameliorate NAFLD in mice by activating the AMPK/ACC pathway and modulating the structure of intestinal flora. [ABSTRACT FROM AUTHOR]