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Updated: Aug 29, 2025

Chinese Herbal Retention Enema for the Treatment of Ulcerative Colitis
Published on: May 16, 2025
Esculentoside A Alleviates Intestinal Dysmotility in Ulcerative Colitis by Regulating H2S/CSE and NO/nNOS Systems.
Ying Liu1, Wenhua Wei2, Shiwei Liang1
1Department of Gastroenterology, Guangxi Health Commission Key Laboratory of Glucose and Lipid Metabolism Disorders, The Second Affiliated Hospital of Guilin Medical University, Guilin, China.
Esculentoside A (EsA) effectively treats ulcerative colitis (UC) by improving intestinal motility and reducing inflammation. This study shows EsA may modulate hydrogen sulfide (H2S) and nitric oxide (NO) pathways in UC treatment.
Area of Science:
- Gastroenterology
- Pharmacology
- Cell Biology
Background:
- Ulcerative colitis (UC) is a prevalent inflammatory bowel disease (IBD).
- Esculentoside A (EsA), a saponin from Phytolacca esculenta, exhibits anti-inflammatory and antioxidative properties.
- The therapeutic potential of EsA in UC remains largely unexplored.
Purpose of the Study:
- To investigate the therapeutic effects of EsA on dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) in a rat model.
- To elucidate the underlying mechanisms involving hydrogen sulfide (H2S)/cystathionine γ-lyase (CSE) and nitric oxide (NO)/neuronal nitric oxide synthase (nNOS) systems.
Main Methods:
- An in vivo UC rat model was established using DSS administration.
- Rats were treated with varying doses of EsA.
- In vitro studies assessed EsA's effects on lipopolysaccharide (LPS)-stimulated primary intestinal neuronal cells.
Main Results:
- EsA treatment improved intestinal motility, body weight, and histological scores in DSS-induced UC rats.
- EsA significantly reduced serum levels of NO and H2S, and suppressed colon tissue expression of CSE, CBS, and nNOS.
- In vitro, EsA protected intestinal neuronal cells from LPS-induced apoptosis and proliferation inhibition, downregulating IL-6, TNF-α, CSE, CBS, and nNOS.
Conclusions:
- EsA demonstrates significant therapeutic potential for ulcerative colitis.
- EsA improves intestinal motility and suppresses inflammation in UC, potentially via modulation of H2S/CSE and NO/nNOS pathways.
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