Traditional Chinese medicine for Helicobacter pylori infection in the antibiotic-resistance era
Ethnopharmacological evidence, mechanisms, and Host–Pathogen modulation
Bibliographic Data
| ID | 24214645 |
|---|---|
| Authors | Kai Zhang (0000-0002-7401-2931), Yu Zhao (0000-0001-9446-644X), Yulei Yang, Yuanyuan Wang (0000-0001-8181-3465), Hongcai Shang (0000-0001-6628-354X), Ji Pu, Min Zhu (0009-0004-6196-8661), Xiangling Zhang (0000-0002-3286-9064), Wen Zhang (0000-0002-8166-2879), JinJing Dou, Mei Zhang (0000-0001-9803-0205) |
| Year | 2027 |
| Volume | 374 |
| Issue | Pt 1 |
| Pages | 122450 |
| Publication date | 2027-02-01 |
| Open Access | Yes |
| Type | ARTICLE |
| Venue | Journal of Ethnopharmacology (JOURNAL) |
| Journal identifiers | ISSN: 0378-8741 • E-ISSN: 1872-7573 |
| Publisher | Elsevier BV (PUBLISHER) |
| DOI | 10.1016/j.jep.2026.122450 |
| PMID | 42810459 |
| OpenAlex | W7214791127 |
| Language | EN |
| References cited | 83 |
ETHNOPHARMACOLOGICAL RELEVANCE: Helicobacter pylori (H. pylori) infection remains a global health burden, and antibiotic resistance has reduced the effectiveness of standard eradication regimens. In traditional Chinese medicine (TCM), persistent infection is interpreted as retention of pathogenic factors in the spleen-stomach system. Herbal formulas are investigated as adjunctive strategies, but their clinical roles and mechanistic basis require clarification. AIM OF THE STUDY: To develop a host-pathogen modulation framework integrating clinical evidence, antibiotic resistance and persistence mechanisms, and TCM pharmacology, while distinguishing clinically supported effects from preclinical plausibility. MATERIALS AND METHODS: This critical narrative review was based on a structured search of six databases from inception through April 2026. Evidence was synthesized without quantitative pooling. RESULTS: Some TCM formulas used with standard regimens were associated with improved eradication outcomes, whereas others showed similar eradication rates with possible advantages in symptom relief, tolerability, or adverse-event reduction. However, confidence in the clinical evidence remains low because most studies were small, single-center trials with heterogeneous interventions and comparators, incomplete risk-of-bias reporting, inconsistent outcome definitions, limited follow-up, and inadequate safety assessment. Preclinical studies suggest that formulas, herbs, and compounds may affect bacterial growth and colonization fitness, urease, adhesion, virulence systems, biofilm-associated tolerance, mucosal injury, inflammation, and gastric-gut microecology. Interpretation of these mechanisms is further limited by inconsistent quantitative pharmacological data, uncertain gastric exposure and pharmacokinetics, and weak linkage between experimental findings and clinical outcomes. CONCLUSIONS: TCM should not replace standard eradication therapy. Its more defensible role is as a potential host-pathogen modulatory strategy with adjunctive, supportive, and mucosa-protective value. The current clinical findings should be regarded as preliminary rather than confirmatory. Rigorous multicenter trials, standardized interventions, quantitative pharmacology, pharmacokinetic validation, and mechanism-linked clinical studies are required.
Antibiotic resistance · ethnopharmacology · Gastritis · Helicobacter pylori infection · herbal medicine mechanism · host-pathogen interaction · Peptic ulcer · Traditional Chinese medicine · Gastrointestinal motility and disorders · Helicobacter pylori-related gastroenterology studies · Medical Research and Treatments
Narrative Reviews
Aqueous extracts and polysaccharides from Liquorice roots (Glycyrrhiza glabra L.) inhibit adhesion of Helicobacter pylori to human gastric mucosa
Sanguinarine, a major alkaloid from Zanthoxylum nitidum (Roxb.) DC., inhibits urease of Helicobacter pylori and jack bean
Coptisine inhibits Helicobacter pylori and reduces the expression of CagA to alleviate host inflammation in vitro and in vivo
Cinnamaldehyde
In-vitro anti-Helicobacter pylori activity and preliminary mechanism of action of Canarium album Raeusch. fruit extracts
Amelioration of Helicobacter pylori-induced gastric injury by Artemisia argyi Folium total extract, its total flavonoids, and eupatilin through suppression of NF-κB signaling and virulence factors
Terminalia chebula Retz. aqueous extract inhibits the Helicobacter pylori-induced inflammatory response by regulating the inflammasome signaling and ER-stress pathway
Dandelion alleviates Helicobacter pylori associated gastritis by inhibiting proteolytic activity of HtrA
| Highly cited | No |
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