Salvia miltiorrhiza (Danshen) is a traditional Chinese herb that is commonly known for its cardiovascular and hepatoprotective benefits. Recent studies have confirmed that Danshen and its bioactive components can influence gut microbial homeostasis, thereby affecting Helicobacter pylori (HP) colonization in the human stomach. HP is a bacterial pathogen associated with various gastrointestinal diseases. Current HP treatments mainly involve antibiotics and proton pump inhibitors. However, their efficacy is strongly compromised by the rapid emergence of antibiotic resistance in HP and genetic heterogeneity among patients. The interaction between Danshen and gut microbial status provides a novel perspective for HP treatment. Understanding the medical properties of Danshen in altering gut microbiota and eliminating HP, as well as the underlying mechanisms, is important for improving human gastrointestinal healthcare. This review investigates the interaction between Danshen and gut microbiota and its impact on HP infection using databases including Web of Science, PubMed, and Google Scholar. We explored the unconventional intersection between Danshen, gut microbiota, and HP infection, shedding light on their intricate interplay and potential therapeutic implications. A comprehensive understanding of this interaction provides valuable insights into developing novel therapeutic strategies that target the gut microbiota to mitigate HP-associated gastrointestinal disorders. Please cite this article as: Li SJ, Miao JX, Wang F, Wang HY, Ma YW, Jiang Y, Xue X. Salvia miltiorrhiza components and gut microbiota interactions in Helicobacter pylori infection. J Integr Med. 2025; 23(5):462-470.
Salvia miltiorrhiza/chemistry* ; Gastrointestinal Microbiome/drug effects* ; Humans ; Helicobacter Infections/microbiology* ; Helicobacter pylori/drug effects* ; Drugs, Chinese Herbal/therapeutic use*

Helicobacter pylori is a bacterium that can cause chronic gastritis, peptic ulcers, and other gastrointestinal diseases. The World Health Organization has classified H. pylori as a group Ⅰ carcinogen. Antibiotics are the primary clinical approach for eradicating H. pylori. However, incomplete eradication of H. pylori by antibiotics can lead to persistent infection, which is a major risk factor for the high incidence of gastric cancer. The widespread use of antibiotics has led to the emergence of multidrug resistance in H. pylori, contributing to treatment failures of chronic gastric diseases and increasing the risk of spreading resistant strains. Multidrug-resistant H. pylori has become a serious challenge in the diagnosis and treatment of gastrointestinal diseases. This paper reviews the global trends in the development of multidrug resistance in H. pylori, the underlying mechanisms, the challenges it poses to clinical diagnosis, and its impact on drug development, drawing on relevant literature and the research findings from our group. It proposes using cgt expression as a novel method for determining viable bacteria, identifying intracellularization as a new form of resistance in H. pylori, and exploring the potential of O-glycans as a therapeutic approach against H. pylori to address multidrug resistance. It provides new insights into understanding the mechanisms of H. pylori multidrug resistance and its prevention strategies, offering promising directions for future clinical treatments and antimicrobial drug development.
Helicobacter pylori/genetics* ; Humans ; Drug Resistance, Multiple, Bacterial ; Helicobacter Infections/microbiology* ; Anti-Bacterial Agents/therapeutic use* ; Gastrointestinal Diseases/drug therapy*

Helicobacter pylori ( H. pylori ) infects approximately half of the population worldwide and causes chronic gastritis, peptic ulcers, and gastric cancer. Test-and-treat strategies have been recommended for the prevention of H. pylori -associated diseases. Advancements in high-throughput sequencing technologies have broadened our understanding of the complex gastrointestinal (GI) microbiota and its role in maintaining host homeostasis. Recently, an increasing number of studies have indicated that the colonization of H. pylori induces dramatic alterations in the gastric microbiota, with a predominance of H. pylori and a reduction in microbial diversity. Dysbiosis of the gut microbiome has also been observed after H. pylori infection, which may play a role in the development of colorectal cancer. However, there is concern regarding the impact of antibiotics on the gut microbiota during H. pylori eradication. In this review, we summarize the current literature concerning how H. pylori infection reshapes the GI microbiota and the underlying mechanisms, including changes in the gastric environment, immune responses, and persistent inflammation. Additionally, the impacts of H. pylori eradication on GI microbial homeostasis and the use of probiotics as adjuvant therapy are also discussed. The shifts in the GI microbiota and their crosstalk with H. pylori  may provide potential targets for H. pylori -related gastric diseases and extragastric manifestations.
Helicobacter Infections/microbiology* ; Humans ; Helicobacter pylori/pathogenicity* ; Gastrointestinal Microbiome/drug effects* ; Probiotics/therapeutic use* ; Anti-Bacterial Agents/therapeutic use*

Inflammatory bowel disease (IBD) is a non-specific inflammatory disease of the gastrointestinal (GI) tract that is generally accepted to be closely related to intestinal dysbiosis in the host. GI infections contribute a key role in the pathogenesis of IBD; however, although the results of recent clinical studies have revealed an inverse correlation between Helicobacter pylori (H. pylori) infection and IBD, the exact mechanism underlying the development of IBD remains unclear. H. pylori, as a star microorganism, has been a focus for decades, and recent preclinical and real-world studies have demonstrated that H. pylori not only affects the changes in the gastric microbiota and microenvironment but also influences the intestinal microbiota, indicating a potential correlation with IBD. Detailed analysis revealed that H. pylori infection increased the diversity of the intestinal microbiota, reduced the abundance of Bacteroidetes, augmented the abundance of Firmicutes, and produced short-chain fatty acid-producing bacteria such as Akkermansia. All these factors may decrease vulnerability to IBD. Further studies investigating the H. pylori-intestinal microbiota metabolite axis should be performed to understand the mechanism underlying the development of IBD.
Chronic Disease ; Dysbiosis/microbiology* ; Gastrointestinal Microbiome ; Helicobacter Infections ; Helicobacter pylori ; Humans ; Inflammatory Bowel Diseases/microbiology* ; Microbiota

Objective To evaluate the gastric microbiome in patients with chronic superficial gastritis (CSG) and intestinal metaplasia (IM) and investigate the influence of Helicobacter pylori (H. pylori) on the gastric microbiome. Methods Gastric mucosa tissue samples were collected from 54 patients with CSG and IM, and the patients were classified into the following four groups based on the state of H. pylori infection and histology: H. pylori-negative CSG (n=24), H. pylori-positive CSG (n=14), H. pylori-negative IM (n=11), and H. pylori-positive IM (n=5). The gastric microbiome was analyzed by 16S rRNA gene sequencing. Results H. pylori strongly influenced the bacterial abundance and diversity regardless of CSG and IM. In H. pylori-positive subjects, the bacterial abundance and diversity were significantly lower than in H. pylori-negative subjects. The H. pylori-negative groups had similar bacterial composition and bacterial abundance. The H. pylori-positive groups also had similar bacterial composition but different bacterial relative abundance. The relative abundance of Neisseria, Streptococcus, Rothia, and Veillonella were richer in the I-HP group than in G-HP group, especially Neisseria (t=175.1, P<0.001). Conclusions The gastric microbial abundance and diversity are lower in H. pylori- infected patients regardless of CSG and IM. Compared to H. pylori-positive CSG group and H. pylori-positive IM, the relative abundance of Neisseria, Streptococcus, Rothia, and Veillonella is higher in H. pylori-positive patients with IM than in H. pylori-positive patients with CSG, especially Neisseria.
Gastric Mucosa/microbiology* ; Gastritis, Atrophic/microbiology* ; Gastrointestinal Microbiome/genetics* ; Helicobacter Infections/microbiology* ; Helicobacter pylori/genetics* ; Humans ; Metaplasia ; RNA, Ribosomal, 16S/genetics* ; Stomach Neoplasms

To investigate the mechanism of long non-coding RNA plasmacytoma variant translocation 1 (PVT1) in gastric cancer caused by (HP) infection. The expression of PVT1 was detected by quantitative real-time polymerase chain reaction in HP-infected normal gastric epithelial cells GES-1. Gastric cancer cell line SGC-7901 was transfected with PVT1 small interfering RNA and co-cultured with HP,and then the inflammatory cytokines such as tumor necrosis factor-α (TNF-α),interleukin (IL) -1β,IL-6 and IL-8 were detected. After PVT1 was knocked down,the effects of PVT1 on the proliferation and migration of gastric cancer cells were examined by cell scratch assay. RNA-pulldown combined with mass spectrometry was used to detect the protein binding to PVT1,and the result of mass spectrometry was verified by RNA-pulldown combined with Western blot. In HP-infected normal gastric epithelial cells GES-1,quantitative real-time polymerase chain reaction showed that PVT1 was significantly up-regulated (=7.160,=0.019). PVT1 was knocked down in gastric cancer cells,and then infected with HP. The expressions of inflammatory factors including TNF-α (=3.899,=0.011),IL-1β (=14.610,=0.000),and IL-8 (=6.557,=0.001) were significantly inhibited. Although PVT1 knockdown had no significant effect on the proliferation ability of gastric cancer cells,it inhibited the migration of cells. PVT1 might interact with RPS8 protein. PVT1 may act as a pro-inflammatory factor and regulate gastric cancer caused by HP infection.
Cell Line, Tumor ; Cell Movement ; Cytokines ; metabolism ; Epithelial Cells ; cytology ; microbiology ; Gene Knockdown Techniques ; Helicobacter Infections ; pathology ; Helicobacter pylori ; Humans ; Inflammation ; RNA, Long Noncoding ; genetics

BACKGROUND: Helicobacter pylori (H. pylori) eradication has been widely used. The recurrence rate of H. pylori after eradication and its related factors are gaining more and more attention. Our study aimed to determine the recurrence rate of H. pylori infection after successful eradication, and analyze its influential factors. METHODS: We prospectively studied 1050 patients with upper gastrointestinal symptoms who were diagnosed as H. pylori infection by gastroscopy and underwent eradication therapies from April 2013 to January 2014. The C-urea breath test (UBT) or Warthin-Starry (WS) staining was done at 8 to 12 weeks after the therapy. Patients with successful eradication were followed by repeated UBT or gastroscopy at one year and 3 years after therapy, as well as, questionnaire surveys. Recurrence was considered if the UBTs or WS staining of biopsy were positive. One-year and 3-year recurrence rates were calculated, and analyzed the differences between recurred patients and others in basic data, sociological characteristics, lifestyle. RESULTS: A total of 743 patients finished the 1-year follow-up, and the 1-year recurrence rate was 1.75%. Of the 607 patients who finished the 3-year follow-up, 28 patients recurred, and the 3-year recurrence rate was 4.61%. Analysis of variance showed that low-income, poor hygiene condition of dining out place, and receiving invasive diagnoses or treatments were significant risk factors for H. pylori infection recurrence. Logistic regression analysis demonstrated that the combination of invasive diagnoses or treatments, the level of income, and the hygiene standard of dining out place were significant and independent influential factors of the recurrence of H. pylori. CONCLUSIONS The 1-year and 3-year recurrence rates of H. pylori infection after eradication therapy are 1.75% and 4.61%. Low-income, poor hygiene condition of dining out place, and a combination of invasive diagnoses or treatments are independent risk factors of H. pylori recurrence.
Adolescent ; Adult ; Aged ; Female ; Gastroscopy ; Helicobacter Infections ; epidemiology ; microbiology ; Helicobacter pylori ; pathogenicity ; Humans ; Incidence ; Logistic Models ; Male ; Middle Aged ; Multivariate Analysis ; Prospective Studies ; Risk Factors ; Surveys and Questionnaires ; Young Adult

ObjectiveGastroscopy combined with gastric mucosa biopsies is currently regarded as a gold standard for diagnosis of gastric cancer. However, its application is restricted in clinical practice due to its invasive property. A new noninvasive population screening process combining the assay of anti-Helicobacter pylori antibody and serum pepsinogen (PG) (ABC method) is adopted to recognize the high-risk patients for further endoscopy examination, avoiding the unnecessary gastroscopy for most population and saving the cost consumption for mass screening annually. Nevertheless, controversies exist for the grouping of ABC method and the intervals of gastroscopy surveillance for each group. In this review, we summarized these popular concerned topics for providing useful references to the healthcare practitioner in clinical practice.

Data SourcesThe PubMed databases were systematically searched from the inception dates to November 22, 2017, using the keywords "Helicobacter pylori," "Pepsinogens," and "Stomach Neoplasms."

Study SelectionOriginal articles and reviews on the topics were selected.

ResultsAnti-H. pylori antibody and serum PG concentration showed significant changes under the different status of H. pylori infection and the progression of atrophic gastritis, which can be used for risk stratification of gastric cancer in clinic. In addition, anti-H. pylori antibody titer can be used for further risk stratification of gastric cancer contributing to determine better endoscopy surveillance interval.

ConclusionsThe early detection and diagnosis of gastric cancer benefit from the risk stratification, but the cutoff values for H. pylori antibody and serum PG concentration require further modification.

Antibodies, Bacterial ; blood ; immunology ; Gastroscopy ; Helicobacter Infections ; blood ; immunology ; Helicobacter pylori ; immunology ; Humans ; Mass Screening ; methods ; Stomach Neoplasms ; blood ; microbiology

Helicobacter pylori (H. pylori) is the causative agent of chronic gastritis and peptic ulcer diseases and is an important risk factor for the development functional dyspepsia, peptic ulceration, gastric adenocarcinoma and mucosa-associated lymphoid tissue lymphoma. H. pylori has very high rates of infection in human populations, and it is estimated that over 50% of the world population is infected. Recently, certain extra-gastric manifestations, linked to H. pylori infection, have been widely investigated. Noteworthy, a growing body of evidences supports an association between H. pylori infection with lung cancer. The present review intend to highlight not only the most recent evidences supporting this association, but also some missed points, which must be considered to validate this emerging association.
Helicobacter Infections ; complications ; Helicobacter pylori ; physiology ; Humans ; Lung Neoplasms ; complications ; microbiology

(Hp) is widely disseminated in human, and Hp infection causes various gastrointestinal diseases, including gastric cancer. Different genotypes of Hp may cause different diseases, so the genotyping is important for clinical and basic research of Hp. This article introduces the methods for Hp genotyping, including multilocus sequence typing, pulsed-field gel electrophoresis, random amplified polymorphic DNA, amplified fragment length polymorphism, and whole-genome sequencing. By reviewing the application of these techniques in Hp genotyping and comparing their advantages and disadvantages, the article provides a theoretical basis for research into the pathogenesis, antibiotic resistance, and epidemiology of Hp infection.
Amplified Fragment Length Polymorphism Analysis ; Genotype ; Helicobacter Infections ; microbiology ; pathology ; Helicobacter pylori ; genetics ; Humans ; Polymerase Chain Reaction ; Research