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World J Gastroenterol. Nov 21, 2026; 32(43): 121477
Published online Nov 21, 2026. doi: 10.3748/wjg.121477
Study on the adhesive effect of deoxyshikonin on Helicobacter pylori
Guang-Fu Pang, Jia-Yin Xu, Ai-Xing Guan, Shi-Xian Yang, Kwanjit Duangsonk, Yan-Qiang Huang, Qi-Hai Zhou, Wen-Ting Zhou
Guang-Fu Pang, Qi-Hai Zhou, College of Physical Education and Health, Guangxi Normal University, Guilin 541006, Guangxi Zhuang Autonomous Region, China
Guang-Fu Pang, School of Medical Technology and Artificial Intelligence, Youjiang Medical University for Nationalities, Baise 533000, Guangxi Zhuang Autonomous Region, China
Jia-Yin Xu, Yan-Qiang Huang, Wen-Ting Zhou, Guangxi Technology Innovation Cooperation Base of Prevention and Control Pathogenic Microbes with Drug Resistance, Youjiang Medical University for Nationalities, Baise 533000, Guangxi Zhuang Autonomous Region, China
Ai-Xing Guan, Department of Gastroenterology, Affiliated Hospital of Youjiang Medical University for Nationalities, Baise 533000, Guangxi Zhuang Autonomous Region, China
Shi-Xian Yang, Guangxi Clinical Medical Research Center for Hepatobiliary Diseases, Affiliated Hospital of Youjiang Medical University for Nationalities, Baise 533000, Guangxi Zhuang Autonomous Region, China
Kwanjit Duangsonk, Wen-Ting Zhou, Department of Microbiology, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand
Yan-Qiang Huang, Wen-Ting Zhou, Guangxi Zhuang Autonomous Region Engineering Research Center of Clinical Prevention and Control Technology and Leading Drug for Microorganisms with Drug Resistance in Border Ethnic Areas, Youjiang Medical University for Nationalities, Baise 533000, Guangxi Zhuang Autonomous Region, China
Qi-Hai Zhou, College of Life Science, Guangxi Normal University, Guilin 541006, Guangxi Zhuang Autonomous Region, China
Co-corresponding authors: Qi-Hai Zhou and Wen-Ting Zhou.
Author contributions: Pang GF and Xu JY contributed equally to experimental work, data acquisition, and original drafting of the manuscript; Guan AX, Yang SX, and Duangsonk K contributed to methodology, materials, and data curation; Huang YQ and Zhou QH contributed to study supervision, project administration, and funding acquisition; Zhou WT conceived the study, supervised the project, interpreted the data, and revised the manuscript critically for important intellectual content; Zhou QH and Zhou WT contributed equally as co-corresponding authors. All authors have read and approved the final manuscript.
AI contribution statement: AI tools (specifically ChatGPT) were used solely for linguistic refinement and formatting assistance. No AI tool was involved in the generation of research data, interpretation of results, or formulation of conclusions. All AI-generated outputs were critically reviewed and revised by the authors.
Supported by Guangxi Science and Technology Major Project, No. AA23073012; National Natural Science Foundation of China, No. 32360035 and No. 32060018; and Guangxi Natural Science Foundation, No. 2025GXNSFHA069251.
Institutional review board statement: This study did not involve human participants, patient data, or human-derived specimens. All Helicobacter pylori strains used in this study were laboratory strains supplied by Professor Bi Hong-Kai. Consequently, institutional review board approval was not required.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Data sharing statement: The datasets generated and/or analyzed during the current study are available from the corresponding author upon reasonable request.
Corresponding author: Wen-Ting Zhou, Guangxi Technology Innovation Cooperation Base of Prevention and Control Pathogenic Microbes with Drug Resistance, Youjiang Medical University for Nationalities, No. 98 Chengxiang Road, Baise 533000, Guangxi Zhuang Autonomous Region, China.
wenting_z@cmu.ac.th
Received: April 14, 2026
Revised: May 11, 2026
Accepted: June 26, 2026
Published online: November 21, 2026
Processing time: 165 Days and 9.1 Hours
BACKGROUND
Helicobacter pylori (H. pylori) infection remains a major etiological factor in chronic gastritis, peptic ulcer disease, and gastric cancer. The increasing prevalence of antibiotic resistance underscores the urgent need for alternative anti-H. pylori agents with clearly characterised molecular targets.
AIM
To investigate whether deoxyshikonin inhibits H. pylori adhesion by modulating urease-associated pathways.
METHODS
Anti-adhesion activity of deoxyshikonin was evaluated in GES-1 and BGC823 cells using Gram staining, fluorescence microscopy, the Alamar Blue Assay, and colony counting. Potential targets were identified using drug affinity-responsive target stability-mass spectrometry and molecular docking. Urease involvement was investigated using reverse transcription-quantitative polymerase chain reaction, western blotting, surface plasmon resonance, phenol red colorimetry, and urease activity assays. A low-urease-expression 26695Δcfa mutant and exogenous urease supplementation were applied for mechanistic validation.
RESULTS
Deoxyshikonin reduced cell-associated H. pylori in a concentration-dependent manner. Molecular docking suggested a stronger binding of deoxyshikonin to UreB than to UreA (-6.1 kcal/mol vs -4.9 kcal/mol). Deoxyshikonin downregulated ureA/ureB and SabA/BabA transcripts; reduced UreB protein abundance; inhibited urease activity; and directly bound to UreB, as demonstrated by surface plasmon resonance analysis (KD = 1.193 μM). The H. pylori 26695Δcfa mutant was less susceptible to deoxyshikonin, whereas exogenous urease promoted bacterial adhesion.
CONCLUSION
Deoxyshikonin inhibits H. pylori adhesion. The current evidence indicates that the urease subunits UreA and UreB are involved as molecular targets in this effect.
Core Tip: Deoxyshikonin exerted dose-responsive anti-adhesion activity against Helicobacter pylori in gastric epithelial cell models. Using an integrated approach combining drug affinity-responsive target stability-mass spectrometry, molecular docking, reverse transcription-quantitative polymerase chain reaction, western blotting, surface plasmon resonance, and urease activity assays, this study identifies urease, particularly UreB, as a key molecular target of deoxyshikonin. The findings further suggest that interference with urease is accompanied by concomitant changes in SabA and BabA expression; however, the precise regulatory mechanism underlying this coordinated response requires further investigation.
