Research progress on the mechanisms of Tibetan medicine Gentianopsis paludosa and its chemical components against ulcerative colitis and associated fibrosis
|更新时间:2026-03-10
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Research progress on the mechanisms of Tibetan medicine Gentianopsis paludosa and its chemical components against ulcerative colitis and associated fibrosis
LI Huan,NIE Qing,AN Yongkang,et al.Research progress on the mechanisms of Tibetan medicine Gentianopsis paludosa and its chemical components against ulcerative colitis and associated fibrosis[J].ZHONGGUO YAOFANG,2026,37(05):676-681.
LI Huan,NIE Qing,AN Yongkang,et al.Research progress on the mechanisms of Tibetan medicine Gentianopsis paludosa and its chemical components against ulcerative colitis and associated fibrosis[J].ZHONGGUO YAOFANG,2026,37(05):676-681. DOI: 10.6039/j.issn.1001-0408.2026.05.22.
Research progress on the mechanisms of Tibetan medicine Gentianopsis paludosa and its chemical components against ulcerative colitis and associated fibrosis
Ulcerative colitis (UC) is a chronic and relapsing inflammatory disease of the intestine. Intestinal fibrosis represents a severe co
mplication and a potential risk factor for malignant transformation.
Gentianopsis paludosa
is one of the traditional Tibetan medicines commonly used for treating gastrointestinal disorders such as damp-heat diarrhea and dysentery. Its chemical composition is complex, encompassing xanthones, flavonoids, terpenoids, and other bioactive components, and it exhibits properties such as clearing heat, eliminating dampness, and detoxifying. This article reviews the research progress on the pharmacodynamic material basis and mechanisms of
G. paludosa
against UC and associated fibrosis. Findings suggest that its extracts (e.g., aqueous extract, ethyl acetate extract) and active constituents (e.g., 1-hydroxy-3,7,8-trimethoxyxanthone, ursolic acid, swertiamarin, luteolin) may inhibit inflammatory cytokines, combat oxidative stress, suppress cell apoptosis, regulate intestinal microbiota and their metabolites, protect the intestinal mucosal barrier, modulate immune responses, and inhibit epithelial-mesenchymal transition, through modulating relevant signaling pathways, such as nuclear factor-kappa B, B-cell lymphoma-2 (Bcl-2)/Bcl-2-associated X protein, and transforming growth factor-β
1
/Smad, thus exerting therapeutic effects against UC and its related fibrosis via these seven aspects.
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XU L , HE B J , SUN Y X , et al . Incidence of inflammatory bowel disease in urban China:a nationwide population-based study [J ] . Clin Gastroenterol Hepatol , 2023 , 21 ( 13 ): 3379 - 3386.e29 .
RIEDER F , MUKHERJEE P K , MASSEY W J , et al . Fibrosis in IBD:from pathogenesis to therapeutic targets [J ] . Gut , 2024 , 73 ( 5 ): 854 - 866 .
MAK J W Y , NG S C . Epidemiology of fibrostenosing inflammatory bowel disease [J ] . J Dig Dis , 2020 , 21 ( 6 ): 332 - 335 .
LATELLA G , DI GREGORIO J , FLATI V , et al . Mechanisms of initiation and progression of intestinal fibrosis in IBD [J ] . Scand J Gastroenterol , 2015 , 50 ( 1 ): 53 - 65 .
LIANG J , YANG H H , CHEN K L , et al . Therapeutic effect of daucosterol on DSS-induced colitis in mice [J ] . BMC Microbiol , 2025 , 26 ( 1 ): 18 .
CHRISTENSEN C , KNUDSEN A , ARNESEN E K , et al . Diet,food,and nutritional exposures and inflammatory bowel disease or progression of disease:an umbrella review [J ] . Adv Nutr , 2024 , 15 ( 5 ): 100219 .
LI B L , DU P L , DU Y , et al . Luteolin alleviates inflammation and modulates gut microbiota in ulcerative colitis rats [J ] . Life Sci , 2021 , 269 : 119008 .
MURO P , ZHANG L , LI S X , et al . The emerging role of oxidative stress in inflammatory bowel disease [J ] . Front Endocrinol , 2024 , 15 : 1390351 .
TRATENŠEK A , LOCATELLI I , GRABNAR I , et al . Oxidative stress-related biomarkers as promising indicators of inflammatory bowel disease activity:a systematic review and meta-analysis [J ] . Redox Biol , 2024 , 77 : 103380 .
VITALE I , PIETROCOLA F , GUILBAUD E , et al . Apoptotic cell death in disease:current understanding of the NCCD 2023 [J ] . Cell Death Differ , 2023 , 30 ( 5 ): 1097 - 1154 .
NEWTON K , STRASSER A , KAYAGAKI N , et al . Cell death [J ] . Cell , 2024 , 187 ( 2 ): 235 - 256 .
MEI C X , MENG F X , WANG X , et al . CD30L is involved in the regulation of the inflammatory response through inducing homing and differentiation of monocytes via CCL2/CCR2 axis and NF-κB pathway in mice with colitis [J ] . Int Immunopharmacol , 2022 , 110 : 108934 .
EKSTEDT N , JAMIOŁ-MILC D , PIECZYŃSKA J . Importance of gut microbiota in patients with inflammatory bowel disease [J ] . Nutrients , 2024 , 16 ( 13 ): 2092 .
NEURATH M F , VIETH M . Different levels of healing in inflammatory bowel diseases:mucosal,histological,transmural,barrier and complete healing [J ] . Gut , 2023 , 72 ( 11 ): 2164 - 2183 .
PARIKH K , ANTANAVICIUTE A , FAWKNER-CORBETT D , et al . Colonic epithelial cell diversity in health and inflammatory bowel disease [J ] . Nature , 2019 , 567 ( 7746 ): 49 - 55 .
FOERSTER E G , MUKHERJEE T , CABRAL-FERNANDES L , et al . How autophagy controls the intestinal epithelial barrier [J ] . Autophagy , 2022 , 18 ( 1 ): 86 - 103 .
LIU J Z , VAN SOMMEREN S , HUANG H L , et al . Association analyses identify 38 susceptibility loci for inflammatory bowel disease and highlight shared genetic risk across populations [J ] . Nat Genet , 2015 , 47 ( 9 ): 979 - 986 .
GEREMIA A , BIANCHERI P , ALLAN P , et al . Innate and adaptive immunity in inflammatory bowel disease [J ] . Autoimmun Rev , 2014 , 13 ( 1 ): 3 - 10 .
WANG Y , LI M , ZHA A S . mTOR promotes an inflammatory response through the HIF1 signaling pathway in ulcerative colitis [J ] . Int Immunopharmacol , 2024 , 134 : 112217 .
LU N H , ZHAO H Q , JING M , et al . The pharmacodynamic active components study of Tibetan medicine Gentianopsis paludosa on ulcerative colitis fibrosis [J ] . Int Immunopharmacol , 2017 , 46 : 163 - 169 .