Research progress on clinical and molecular mechanisms of Xianglian pills in the treatment of ulcerative colitis
- VernacularTitle:香连丸治疗溃疡性结肠炎的临床及分子机制研究进展
- Author:
Ying LI
1
;
Zaoyu ZHANG
1
;
Rong DENG
1
;
Jiale CHEN
1
;
Yanlong LI
2
Author Information
1. School of Integrated Traditional Chinese and Western Medicine，Gansu University of Chinese Medicine，Lanzhou 730000，China
2. Spleen and Stomach Disease Diagnosis and Treatment Center，Gansu Provincial Hospital of Traditional Chinese Medicine，Lanzhou 730050，China
- Publication Type:Journal Article
- Keywords:
Xianglian pills;
ulcerative colitis;
clinical research;
molecular mechanism;
research progress
- From:
China Pharmacy
2025;36(20):2609-2614
- CountryChina
- Language:Chinese
-
Abstract:
Ulcerative colitis （UC） is a chronic intestinal autoimmune disease， with clinical manifestations including abdominal pain， diarrhea， mucus and bloody stools， and its pathogenesis is complex. The classic prescription Xianglian pills （XLP） has been widely used in the clinical treatment of UC in recent years. It has few adverse reactions， good patient tolerance， and shows significant potential for clinical application. However， there is currently no comprehensive integration of evidence on its clinical research and molecular mechanisms. Through a systematic review of the clinical research and molecular mechanisms of XLP in the treatment of UC， it is found that XLP and its modified formulas， when used in combination with chemical drugs， can significantly improve the symptoms of UC patients and reduce intestinal inflammation， with superior efficacy compared to chemical drugs alone. Its mechanism of action involves regulating pan-apoptosis， immune response， signaling pathways （hypoxia-inducible factor-1α， nuclear factor-κB， etc.）， intestinal flora， and repairing the intestinal mucosal barrier. Its medicinal materials， monomers and active components can also prevent the differentiation of helper T cells 17 and restore the balance of M1/M2 cells through regulating multiple pathways such as Wnt/β -catenin and Janus kinase/signal transducer and activator of transcription， thereby reducing intestinal damage in UC.
