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Review Article
1 (
2
); 88-97
doi:
10.25259/STN_21_2025

Translational Potential of Plant-Derived Therapeutics in Combating Helicobacter Pylori and Antibiotic Resistance

1Department of Natural Products and Alternative Medicine, King Abdulaziz University Jeddah, Saudi Arabia.
Author image

* Corresponding author: Prof. Hossam M. Abdallah Department of Natural Products and Alternative Medicine, King Abdulaziz University Jeddah, Saudi Arabia. hmafifi2013@gmail.com

Received: , Accepted: ,
© 2025 Published by Scientific Scholar on behalf of Science and Technology Nexus
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This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-Share Alike 4.0 License, which allows others to remix, transform, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

How to cite this article: Abdallah HM. Translational Potential of Plant-Derived Therapeutics in Combating Helicobacter Pylori and Antibiotic Resistance. Sci Technol Nex 2025;1:88-0. doi: 10.25259/STN_21_2025

Abstract

This review highlights the potential of plant-derived natural products in combating Helicobacter pylori infection amid rising antibiotic resistance. A comprehensive literature search was conducted in PubMed, Scopus, Web of Science, and Google Scholar (2005–2025), using keywords related to natural products, phytochemicals, and anti-H. pylori activity. Eligible studies included in vitro, in vivo, and clinical investigations addressing antibacterial, anti-adhesion, anti-virulence, and anti-inflammatory effects. Alkaloids, flavonoids, terpenoids, tannins, and volatile oils demonstrated multi-targeted actions, including urease inhibition, suppression of adhesion and motility, downregulation of virulence factors (CagA, VacA), membrane disruption, and immune modulation. Several compounds enhance antibiotic efficacy, reducing resistance. Clinical studies on agents such as Nigella sativa, licorice, broccoli sprouts, and curcumin showed improved eradication rates, reduced oxidative stress, and symptom relief. Plant-based natural products represent promising adjuncts to conventional therapies. Further well-designed clinical trials and advanced delivery systems are needed to establish their clinical utility.

Keywords

Helicobacter pylori
Natural products
Phytochemicals
Urease inhibitors

1. INTRODUCTION

Helicobacter pylori (H. pylori) is a spiral-shaped, Gram-negative, microaerophilic bacterium that colonises the human gastric mucosa and is recognised as a major cause of gastrointestinal diseases, including chronic gastritis, peptic ulcers, mucosa-associated lymphoid tissue (MALT) lymphoma, and gastric cancer.[1] Identified in 1983, H. pylori is now classified as a Group I carcinogen by the World Health Organisation due to its strong association with gastric malignancies.[2] H. pylori infects over half of the global population, with prevalence rates exceeding 80% in developing countries compared to 30–50% in developed regions.[1] Transmission occurs primarily via fecal–oral and oral–oral routes, often facilitated by poor hygiene, overcrowded living conditions, contaminated water sources, and close human contact, particularly in childhood.[3]

The pathogenicity of H. pylori is driven by several virulence factors, notably, urease, flagella, adhesins, the cytotoxin-associated gene A (CagA) and vacuolating cytotoxin A (VacA). CagA disrupts cellular signaling, promoting inflammation and oncogenesis, while VacA causes epithelial cell damage, apoptosis, and immune evasion.[4] These factors enable the bacterium to persist in the acidic gastric environment by producing urease, which neutralizes stomach acid.

The standard treatment for H. pylori involves triple therapy, combining a proton pump inhibitor (PPI) with two antibiotics; commonly clarithromycin and amoxicillin or metronidazole. However, the global rise in antibiotic resistance, especially to clarithromycin and metronidazole, has significantly reduced the efficacy of this approach. Resistance rates for clarithromycin exceed 40% in some regions, and eradication rates of triple therapy have fallen below 80%, which is considered suboptimal.[5] Additionally, triple therapy is associated with gastrointestinal side effects, poor compliance, and the risk of microbiota disruption.[5]

In response to growing antibiotic resistance and therapy failure, there is increasing interest in natural products and plant-based therapies as alternative or complementary treatments. Phytochemicals such as alkaloids, flavonoids, polyphenols and terpenoids have shown promising anti-H. pylori, anti-inflammatory, and gastroprotective effects in both in vitro and in vivo models.[6] These compounds can inhibit bacterial urease activity, reduce adhesion to gastric cells, modulate immune responses, and protect mucosal integrity. For example, flavonoid-rich extracts containing quercetin, catechin, and rutin exhibit multiple mechanisms including urease inhibition and oxidative stress reduction.[7] The use of phytotherapy not only addresses the challenge of resistance but also offers fewer side effects and broader acceptance in many cultures, especially where herbal medicine has a long-standing history of use.[8]

Given the rising tide of antibiotic resistance and the chronic nature of H. pylori infection, exploring plant-based therapeutic agents offers a promising, sustainable, and safer alternative. This review aims to synthesize the current scientific literature on plant extracts and phytoconstituents in the management of H. pylori infection, evaluating their efficacy, mechanisms of action, and potential integration into clinical practice.

2. METHODOLOGY

To collect relevant literature on natural products with anti-Helicobacter pylori activity, an extensive search was performed using major scientific databases including PubMed, Scopus, Web of Science, and Google Scholar. The search covered the period from 2005 to August 2025 and employed specific keywords such as “natural products + Helicobacter pylori,” “plant extracts + anti-H. pylori,” “phytochemicals + anti-H. pylori,” “terpenoids/flavonoids/alkaloids + H. pylori inhibition,” and “medicinal plants + anti-urease/anti-biofilm/anti-virulence.” Additional filters were applied to include both in vitro, in vivo, and clinical studies that highlight the antibacterial, anti-adhesion, anti-biofilm, and anti-virulence properties of natural products against H. pylori.

3. RESULTS

3.1. Anti-H. pylori mechanisms

Medicinal plants exert anti-H. pylori effects through a variety of synergistic mechanisms that target the bacterium’s survival, colonisation, and pathogenicity. One major mechanism involves disrupting the bacterial envelope structure, which compromises membrane integrity, inhibits biofilm and outer membrane vesicle formation, and impairs nutrient transport seen with compounds like coptisine,[9] safflower extract,[10] and propolis.[11]

Another key strategy is the inhibition of bacterial adhesion to gastric epithelial cells by targeting adhesion molecules such as BabA, SabA, and OipA; plant extracts from turmeric,[12] cranberry,[13] parsley,[12] and Syzygium aromaticum[14] have shown efficacy in this area.

Some phytochemicals interfere directly with DNA replication and transcription by inhibiting DNA gyrase and topoisomerase, as observed with emodin,[15] cinnamaldehyde,[16] and licorice-derived compounds.[17]

Additionally, certain compounds disrupt redox reactions within the bacteria, leading to oxidative stress and cell death, exemplified by 2-Methoxy-1,4- Naphthoquinone from Impatiens balsamina.[18] These plant-based agents also impact other bacterial survival factors, including protein synthesis, motility, and virulence gene expression (e.g., cagA, vacA), and they can modulate the host immune response by reducing pro-inflammatory markers like IL-8, TNF-α, and COX-2. Notable anti-H. pylori compounds include tea catechins (especially Epigallocatechin Gallate; EGCG), curcumin, anthocyanins, and protoberberine alkaloids such as berberine and coptisine, all of which exhibit multi-targeted actions.[19]

Urease inhibition [Figure 1] is also a prominent mechanism, as urease helps H. pylori to neutralise stomach acid. Several plant extracts, natural compounds, and novel formulations have demonstrated significant anti-H. pylori and urease inhibitory activities. Acetone and methanol extracts of Acacia nilotica and Calotropis procera exhibited strong activity within a range of 4.0–256 μg/mL, while isolated compounds from Oliveria decumbens such as stigmasterol, tiliroside, and carvacrol particularly in the hexane fraction, proved highly effective at concentrations between 0.27–0.7 mM, with carvacrol and stigmasterol being the major contributors. Also, olive extract and Zanthoxylum nitidum[20] inactivate urease in a concentration-dependent manner. Alkaloids from Rhizoma Coptidis, especially coptisine, inhibited urease maturation by interfering with UreG (urease accessory protein) activity.[21] Another protoberberine alkaloid, epiberberine, acted as an uncompetitive inhibitor for H. pylori urease and a competitive inhibitor for jack bean urease in a slow-binding, concentration-dependent manner (2.3–3 μM).[21] Evodiamine from Evodia rutaecarpa (20 μM) reduced T4SS (Type IV Secretion System) and SecA (Secretion protein A) protein expression, limiting CagA and VacA translocation and suppressing Mitogen-Activated Protein Kinase pathway/Nuclear Factor kappa B (MAPK/NF-κB) activation, thereby decreasing IL-8 secretion.[21] The citrus flavanone hesperetin showed broad-spectrum anti-H. pylori activity at 50 μM, including suppression of replication, transcription, motility, adhesion, and urease-related genes, along with inhibition of CagA and VacA translocation.[21] Qing Guo extracts, both aqueous and ethyl acetate, exhibited Minimum Inhibitory Concentration (MIC) values of 39–625 μg/mL and MBC (Minimum Bactericidal Concentration) values of 78–1250 μg/mL, inducing morphological changes, urease inhibition, and downregulation of vacA and cagA virulence genes. Several flavonoids chrysin, galangin, kaempferol, luteolin, morin, and quercetin showed strong urease binding affinity, surpassing the standard inhibitor AHA (Acetohydroxamic acid), with quercetin emerging as a potent noncompetitive urease inhibitor at 11.2 μM. Additionally, hesperetin-7-rhamnoglucoside isolated from citrus peel inhibited urease competitively in a concentration-dependent manner (40.6 mM), causing bacterial membrane disruption and amino acid leakage.[21] Zerumbone from Zingiber zerumbet disrupted urease activity at 50–100 μM without affecting transcription or expression of urease A and B, suggesting the formation of inactive urease–zerumbone complexes. Anthraquinones and their glucosides from Rumex acetosa, including chrysophanol-8-O-β-d-glucoside, showed strong anti-H. pylori activity (IC50 8.60 μM; MIC 15.7 μM). Laurus nobilis leaf extract, enriched in phenolics and flavonoids such as gallic acid, rutin, quercetin, and hesperetin, exhibited potent anti-urease activity (MIC 34.17 μg/mL; MBC 1.9 μg/mL). From Zanthoxylum armatum DC, chlorogenic acid (IC50 57.67 mg/mL) demonstrated strong interaction with H. pylori urease.[21] Coumarins isolated from Citrus sinensis leaves; bergapten, xanthotoxin, and citropten were identified as active anti-H. pylori, with citropten showing potent activity (MIC 2.4 μM, MBC 3.9 μg/mL).

Anti-H. pylori mechanisms of plant derived compounds. H. pylori: Helicobacter pylori; NF-κB: Nuclear Factor kappa B; IL-8: Interleukin-8; COX-2: Cyclooxygenase-2; CagA: Cytotoxin-Associated Gene A; VacA: Vacuolating Cytotoxin A
Figure 1:
Anti-H. pylori mechanisms of plant derived compounds. H. pylori: Helicobacter pylori; NF-κB: Nuclear Factor kappa B; IL-8: Interleukin-8; COX-2: Cyclooxygenase-2; CagA: Cytotoxin-Associated Gene A; VacA: Vacuolating Cytotoxin A

Innovative approaches using nanoparticles also revealed that silver nanoparticles synthesized with Ficus carica extract inhibited urease, reducing ammonia release to 16% (comparable to thiourea at 3.87%), while Silver (Ag) Nanoparticles (AgNPs) derived from Solanum xanthocarpum berries exhibited MIC values of 2–8 μg/mL, proving more potent than silver nitrate and even some standard antibiotics like metronidazole.

3.2. Plant extracts with anti-H. pylori activity

Screening of commercial oils containing plants revealed that lemongrass, cedarwood, thyme, lemon balm, and basil oils possess the strongest inhibitory activity.[22] Several species-containing oils, including Thymus serpyllum (MIC 2.0–4.0 μl/ml)[23] and other thymus species showed potent activity against H. pylori like T. capitatus and T. carmanicus.[24] T. caramanicus, have exhibited strong growth inhibition against multiple resistant clinical isolates, with inhibition zones ranging from 50 to 65 mm.[25] Other genera as Oliveria decumbens, Lippia citriodora (lemon verbena), and Cymbopogon citratus (lemongrass), demonstrated strong bactericidal activity against H. pylori.[26] Also, some Cinnamomum species like C. zeylanicum bark essential oil (EO) (rich in cinnamaldehyde and eugenol) displayed significant bactericidal activity (MBC 40 μg/mL). Meanwhile, Other species rich in 1,8-cineole (eucalyptol), like C. glanduliferum, Eucalyptus globulus, and Melaleuca spp., also showed potent effects (MIC 31–46 μg/mL).[24] Paeonia lactiflora root EO induced abnormal morphological changes, converting spiral cells into irregular coccoid forms lacking flagella.[27]

H. pylori relies on adhesins to bind gastric epithelial cells and on biofilm formation to persist and resist host defenses and antimicrobials. Disruption of these processes can reduce colonisation and infection. The EO of Origanum minutiflorum significantly reduced adhesion of H. pylori to gastric cells (over 80% reduction). Although many EOs exhibit anti-biofilm activity against other pathogens (e.g., S. aureus, E. coli, P. aeruginosa), evidence specific to H. pylori is limited. Notably, the EO of Atractylodes lancea inhibited biofilm formation at sub-MIC concentrations. Overall, plant EOs show promise in impairing both the adhesive capacity and biofilm formation of H. pylori, but more targeted studies are required to confirm their full potential.[24] Moreover, several plant EOs and their constituents have demonstrated strong anti-urease activity. Essential oils, such as cedarwood, demonstrated strong anti-urease activity against clinical H. pylori strains (MIC 5.3 mg/L, MBC 15.6 mg/L), often through noncompetitive inhibition,[28] where both substrate and inhibitor bind simultaneously but independently to the enzyme. EOs from Juniperus virginiana and Pinus silvestris displayed the strongest inhibition (IC₅₀ = 5.3 and 18.4 μg/mL), while Citrus limon, Abies alba, Melaleuca alternifolia, and Cymbopogon schoenanthus showed moderate activity, and Origanum vulgare and Thymus vulgaris oils exhibited little to no urease inhibition despite strong growth-inhibitory effects, suggesting different mechanisms of action.[22]

Several volatile oil–containing plants have demonstrated potent in vivo activity. Pistacia lentiscus resin has shown anti-H. pylori activity in humans, with reported MIC values ranging from 275–1100 µg/mL. The major bioactive constituents identified were α-pinene (93.17%), β-pinene (1.69%), limonene (0.59%), camphene (0.57%), and myrcene (0.47%).[29] Cinnamomum cassia bark demonstrated activity in Mongolian gerbils, with a MIC of 0.3 μL/mL. Its main constituent, cinnamaldehyde (74%), along with linalool (3.9%), cinnamyl acetate (3.8%), and α-caryophyllene (5.3%), are believed to contribute to its anti-H. pylori effect.[30] Nigella sativa seeds also showed significant efficacy in humans while, Lemongrass demonstrated promising results in mice models, against H. pylori infection.[31,32]

Beyond these EO containing plants, several other medicinal plants were reported to inhibit H. pylori urease activity, including Acacia nilotica, Casuarina equisetifolia, Calotropis procera, Camellia sinensis, and Fagonia arabica.[32,33]

Furthermore, extracts such as Zingiber officinale, Curcuma amada (together with C. longa), and Impatiens balsamina demonstrated antimicrobial activity against antibiotic-resistant H. pylori strains and acted synergistically with clarithromycin, highlighting their potential for combination therapy.[34,35]

In addition, several medicinal plants and their extracts have demonstrated in vivo potent activity against H. pylori. Brassica oleracea seeds demonstrated significant anti-H. pylori effects in mice, though their specific active constituents.[36] Liquorice extract showed in vitro and in vivo anti-H. pylori potential due to its variable constituents. Flavonoids and isoflavones such as glabridin, licochalcone A, licoricidin, galbrene, and licoisoflavone B exhibited strong antibacterial effects against H. pylori, including antibiotic-resistant strains, mainly through inhibition of protein synthesis, DNA gyrase, and dihydrofolate reductase, while licorice polysaccharides specifically reduced bacterial adhesion. Clinical studies further suggest licorice extracts enhance eradication rates when combined with standard clarithromycin-based triple therapy. However, safety concerns arise from glycyrrhizin, which may induce mineralocorticoid-like side effects (oedema, hypertension, electrolyte imbalance). Modified low-glycyrrhizin preparations significantly mitigate these risks, enhancing licorice’s therapeutic potential.[19,37,38] Curcuma longa (roots and rhizomes) displayed anti-H. pylori activity in mice due to its major curcumin content in H. pylori-infected C57BL/6 mice.[39] Coptis chinensis root showed efficacy in rat models of H. pylori infection, adding to the evidence for protoberberine alkaloids in targeting this pathogen.[40] Camellia sinensis (green tea) exhibited urease inhibitory activity in mice, which is a key mechanism for reducing bacterial survival in the gastric environment.[41] Allium sativum cloves (garlic) also showed efficacy in Mongolian gerbils, with MIC values ranging from 8–32 μg/mL. The activity is attributed mainly to sulfur-containing compounds, including diallyl trisulfide (33.4%), diallyl disulfide (20.8%), and allyl methyl trisulfide (19.2%).[42] Finally, Vaccinium macrocarpon fruits (cranberry) displayed inhibitory effects in humans, supporting its role as a natural anti-H. pylori agent.[43]

3.3. Phytoconstituents in treatment of H. pylori infection

3.3.1. Terpenes

Monoterpenes and sesquiterpenes in volatile oils

Volatile oils, commonly referred to as essential oils (EOs), are complex mixtures of aromatic and volatile secondary metabolites derived from plants. They have long been recognised for their broad-spectrum antimicrobial properties, including activity against H. pylori.[32] Volatile oils offer a promising natural alternative to conventional antibiotic due to their multi-targeted mechanisms of action and low propensity for resistance development.[32] Numerous plant-derived essential oils isolates have shown significant in vitro antibacterial activity against H. pylori strains, including antibiotic-resistant isolates.

Key active constituents of essential oils with anti-H. pylori activity include several phenylpropanoids, monoterpenes, alcohols, and sesquiterpenes. Among phenylpropanoids, cinnamaldehyde and eugenol were the most potent (MIC 1 μg/mL), with isoeugenol showing stronger bactericidal activity (MBC 40 μg/mL) than eugenol (MBC 100 μg/mL), while methyl chavicol (estragole) and methyl eugenol were weaker. Within monoterpenes, thymol (MIC 7.8 μg/mL), carvacrol (20 μg/mL), menthol (15.6 μg/mL), and citral (40 μg/mL) were effective, though Mentha piperita EO was less active than isolated menthol. Among sesquiterpenes, α-bisabolol and bisabolol oxide B (from Plinia cerrocampanensis) showed strong effects, while Juniperus virginiana EO rich in α-cedrene, thujopsene, and cedrol was also highly active; in contrast, β-caryophyllene, α-/β-pinene, and β-myrcene exhibited weaker individual activity but contributed synergistically within EOs. Other compounds such as citral, the major active in lemongrass and related species demonstrated notable antibacterial effects against H. pylori.[24,44] Within monoterpenoids, activity varies with chemical groups: hydrocarbon-dominant monoterpenes are weakly active, while those with alcohol or aldehyde groups (e.g., lemongrass and lemon oils) exhibit the highest anti-H. pylori activity.[44]

The hydrophobic nature of volatile oils enables them to penetrate phospholipid membranes, disrupt lipid structures, collapsing proton motive force, and impairing pH homeostasis. This leads to leakage of cellular ions and metabolites, ATP depletion, and ultimately bacterial cell death.[45,46] Compounds such as carvacrol, isoeugenol, nerol, citral, and sabinene show particularly potent anti-H. pylori activity [Supplementary Figure 1].[44] Meanwhile, thymol damages cytoplasmic membranes through its hydroxyl group and delocalized electrons, altering permeability and causing potassium and ATP leakage.[46] Carvacrol disrupts and depolarises membranes, depletes intracellular ATP, and induces leakage, although its effect diminishes when combined with thymol.[47]

Supplementary Figure 1

The spiral shape and flagella of H. pylori are vital for penetrating gastric mucus and colonising the stomach epithelium. Several plant essential oils and their constituents disrupt these features, impairing infection. Compounds such as eugenol, cinnamaldehyde, and patchouli alcohol similarly promoted transformation to coccoid forms, while also damaging the cell wall and cytoplasmic membrane.[48,49] In another study, immobilised eugenol, vanillin, and carvacrol on silica microparticles caused complete loss of spiral forms within 24 hours, with coccoid or short bacilli forms predominating.[50] These agents likely act by attaching to the cell surface, disrupting membrane integrity, causing leakage of ions and metabolites, loss of energy substrates, and ultimately cell death.[24]

Patchouli alcohol, a tricyclic sesquiterpenoid, significantly reduced bacterial motility by impairing or completely preventing flagella formation.[49] Beyond its effect on motility, patchouli alcohol also inhibited urease activity[51] and bacterial adhesion to gastric epithelial cells in a dose-dependent manner.[24] In addition, other natural terpenoids have shown promising anti-H. pylori activity. For instance, β-caryophyllene suppressed bacterial growth in vivo (on Mongolian gerbils) and in vitro by downregulating DNA replication genes and virulence factors such as CagA and VacA,[52] while geraniol exhibited potent antimicrobial activity with a MIC of 0.53 mg/L.[53]

Among individual compounds, α- and β-pinene, β-myrcene, and β-caryophyllene showed weak urease inhibition, though some possess gastroprotective properties or can reduce H. pylori colonisation and virulence gene expression.[24] In addition, thymoquinone, dihydrothymoquinone, from Nigella sativa;[54] terpinene 4-ol, pyrrolidine, aromadendrene, and α-gurjunene from Sclerocarya birrea[55] displayed potent urease inhibitory activity.

Diterpene; Ovatodiolide (OVT), a diterpenoid lactone isolated from Anisomeles indica, has demonstrated potent bactericidal activity against both reference and multidrug-resistant strains of Helicobacter pylori. In an in vitro infection model, it significantly inhibited bacterial adhesion to and invasion of human gastric epithelial cells (AGS). Beyond its direct antibacterial effects, OVT suppressed H. pylori-induced inflammatory responses by reducing nuclear factor (NF)-κB activation and lowering interleukin-8 (IL-8) expression in infected AGS cells. Moreover, OVT attenuated the activity of the cytotoxin-associated gene A (CagA) by decreasing its translocation and phosphorylation, thereby preventing the development of the characteristic hummingbird phenotype in AGS cells.[56]

Triterpenoids also show potent anti-H. pylori activity. Glycyrrhizic acid [Supplementary Figure 2] from Glycyrrhiza glabra serving as a representative example. Its metabolite, glycyrrhetinic acid, rapidly inhibits H. pylori growth and displays cytotoxic effects against the pathogen. However, the long-term use of triterpene glycosides (saponins) must be approached with caution due to their mineralocorticoid effects. Thus, while triterpenoid-rich plants remain important in ethnomedicine for ulcer treatment, their safety requires careful evaluation.[57]

Supplementary Figure 2

Tetraterpenoids (carotenoids), consisting of 40-carbon backbones, contribute primarily through antioxidant and anti-inflammatory mechanisms [Supplementary Figure 2]. β-Carotene, abundant in orange-coloured fruits and vegetables, suppresses H. pylori-induced oxidative stress by inhibiting Nicotinamide Adenine Dinucleotide Phosphate (reduced form) (NADPH) oxidase, reducing reactive oxygen species (ROS) generation, and downregulating inflammatory mediators such as iNOS and COX-2.[58] It also attenuates ROS-driven signalling pathways (MAPKs and NF-κB), thereby reducing inflammatory damage. However, despite its strong antioxidant potential, β-carotene has not been conclusively shown to exhibit direct antimicrobial activity against H. pylori, with most studies focusing on its role in gastric cancer prevention. In contrast, astaxanthin, a xanthophyll carotenoid found in crustaceans like shrimp and lobster, displays ten-fold stronger antioxidant activity than β-carotene and shows robust anti-H. pylori potential. Animal studies have demonstrated that astaxanthin-rich diets inhibit H. pylori colonisation and inflammation in gastric tissues, while mechanistic studies reveal that it reduces oxidative stress, shifts the Th1/Th2 immune response to favor bacterial clearance, and inhibits H+,K+-ATPase, a key enzyme in gastric acid regulation.[59] These combined effects highlight astaxanthin as a particularly promising candidate among carotenoids.[60] Previous studies have indicated that higher dietary intake of lycopene, particularly from sources such as tomatoes and tomato-based products (e.g., tomato ketchup), is inversely associated with the risk of gastric ulcers and with H. pylori infection. Moreover, lycopene itself has been reported to exhibit potent anti-H. pylori activity.[61]

3.3.2. Alkaloids

Alkaloids represent a diverse class of natural products with notable anti-H. pylori activities, acting through multiple mechanisms. Aminosterol alkaloid, disrupts the bacterial cell membrane, creating additional portals for antibiotic entry. This property makes it particularly valuable in synergistic therapy with conventional drugs such as amoxicillin, enhancing bacterial eradication efficiency.[60] Another important alkaloid, piperine from black pepper, reduces H. pylori motility and adhesion to gastric epithelial cells, thereby suppressing colonisation and infection progression.[62]

Among alkaloid subclasses, protoberberine alkaloids [Supplementary Figure 3] notably berberine, coptisine, palmatine, epiberberine, jatrorrhizine, and berberrubine, collectively known as “Coptis alkaloids” from Coptis chinensis—have been extensively studied. These tetracyclic benzyl-tetrahydroisoquinolines display broad pharmacological activities, with coptisine and berberine showing the strongest anti-H. pylori activity (MIC 16–50 μg/mL),[63] palmatine exhibiting moderate potency,[64] and epiberberine[65] and jatrorrhizine weaker inhibition.[19] Structural modifications, such as 8-octylberberine, markedly enhance efficacy, achieving MICs as low as 0.25–0.5 μg/mL. Their mechanisms of action are multifaceted: inhibition of urease (via catalytic centre, UreG-mediated maturation, or ureB subunit binding), membrane destabilisation, suppression of virulence gene transcription, impairment of flagella, inhibition of OMP (Outer Membrane Proteins) transport proteins (SecA, BamD), and prevention of adhesion. Beyond antibacterial effects, protoberberines exert potent anti-inflammatory actions by downregulating CagA, reducing urease-induced apoptosis, alleviating gastritis, inhibiting Epidermal Growth Factor Receptor (EGFR) ligands, scavenging free radicals, and attenuating MAPK and NF-κB signaling. While preclinical evidence strongly supports their therapeutic potential, the clinical efficacy of protoberberine alkaloids against H. pylori remains to be fully established.[19]

Supplementary Figure 3

3.3.3. Phenolic compounds

Simple phenolic compounds: Resveratrol [Supplementary Figure 4], demonstrates promising anti-H. pylori activity through alteration of bacterial membrane structure and permeability, inhibition of urease, ROS generation, and interference with intracellular functions, including translation, outer membrane proteins, transport proteins, and ATP synthase.[19,66] In addition, curcumin [Supplementary Figure 4], the main constituent of Curcuma longa rhizomes, exerts anti-H. pylori activity through different mechanisms. It directly inhibits bacterial growth with MIC values ranging from 5–50 μg/mL, primarily by non-competitive inhibition of shikimate dehydrogenase (SDH) (IC₅₀ ≈ 15.4 μM), disrupting the shikimate pathway. In addition to antibacterial activity, curcumin exerts anti-inflammatory and protective effects. It reduces H. pylori-induced activation of NF-κB, MMP-3, and MMP-9, upregulates Indoleamine 2,3-Dioxygenase (IDO) expression, lowers IL-17 levels, and restores 15-PGDH expression via the ERK–JNK–AP-1 pathway, thereby reducing inflammation and potentially preventing gastric carcinogenesis.[67-69] Curcumin also preserves membrane stability, preventing bacterial escape and spread within host tissues.[19]

Supplementary Figure 4

Flavonoids: Natural flavonoids have demonstrated strong antimicrobial and anti-virulence activity against H. pylori, with several purified compounds such as apigenin, kaempferol,[70] hesperetin,[71] quercetin,[72] nobiletin,[73] baicalin, and its aglycon baicalein,[74] and genistein[75] [Supplementary Figure 5], showing potent in vitro activity (MIC ≤ 8 μg/mL) comparable to conventional antibiotics.[19] Their mechanisms are multifactorial, including direct antimicrobial action through inhibition of essential bacterial regulators like HsrA, disruption of enzymes, secretion systems, and membranes, with their hydroxyl groups playing a key role in potent anti-urease activity. They also exert anti-virulence effects by suppressing major virulence factors such as CagA and VacA, thereby reducing NF-κB activation, pro-inflammatory cytokine release (IL-8, TNF-α, IL-1β), oxidative stress, apoptosis, and gastric mucosal damage. In addition, flavonoids provide anti-inflammatory protection by alleviating gastric inflammation, reducing vacuolation and lipid peroxidation, and downregulating key signaling pathways like p38 MAPK and NF-κB. Importantly, they act synergistically with standard antibiotics (CLR, MTZ, AMX, TET, LVX), often through inhibition of efflux pump genes such as hefA or by preventing morphological transitions that enhance resistance. Collectively, these combined bactericidal, anti-virulence, anti-inflammatory, and synergistic properties highlight flavonoids as promising candidates for novel H. pylori therapies.[76]

Supplementary Figure 5

Catechins: Tea catechins, a group of flavonoid polyphenols including catechin (C), epicatechin (EC), gallocatechin (GC), epigallocatechin (EGC), catechin gallate (CG), epicatechin gallate (ECG), gallocatechin gallate (GCG), and epigallocatechin gallate (EGCG) [Supplementary Figure 6], are well known for their strong antioxidant properties such as metal ion chelation, ROS scavenging, and inhibition of oxidase enzymes.[77] Beyond antioxidant effects, catechins demonstrate notable antibacterial activity by disrupting bacterial membranes, forming complexes with cell walls, suppressing hydrogen peroxide production, and interfering with material exchange.[77] Multiple studies confirm their anti-H. pylori activity, with mechanisms including urease inhibition, genetic damage, protein synthesis inhibition, and reduced adhesion.[78] Among them, EGCG exhibits the strongest activity (MIC 8 μg/mL).[79] Both green tea extracts and red tea components have shown in vivo efficacy in reducing colonisation and improving gastric inflammation and lesions in animal models.[80] Importantly, catechins selectively inhibit H. pylori without disturbing beneficial gut flora and may also mitigate complications, such as by regulating the PI3K/AKT pathway to suppress gastric cancer cell proliferation, induce apoptosis, and modulate the cell cycle.[77] Synergistic therapies enhance their effectiveness: combinations with sucralfate or sialic acid significantly reduced infection in animal models, with additive effects on oxidative stress, inflammation, and autophagy regulation.[81] Furthermore, nanotechnology-based delivery systems (e.g., EGCG–fucose–carboxymethyl chitosan–gold nanoparticles) have been developed to overcome catechins’ limitations of poor stability, low bioavailability, and short gastric retention.[19,82]

Supplementary Figure 6

Anthocyanins: They are water-soluble flavonoids responsible for the red, purple, and blue colours in many fruits, berries, and vegetables, are potent natural antioxidants with broad biomedical properties, including antibacterial, antiviral, anticancer, and protective effects on DNA, immunity, and multiple organ systems.[83,84] Several studies highlight their inhibitory activity against H. pylori.[85] Berry extracts (raspberry, blueberry, cranberry, elderberry, strawberry, and bilberry) significantly suppressed H. pylori growth in vitro, with cranberry juice shown to improve clearance rates in women when added to triple therapy, likely by reducing bacterial adhesion.[86] Black raspberry extracts displayed the strongest inhibitory activity in vitro without harming gastric cells,[87] and cranberry rich in A-type proanthocyanidins and anthocyanins, was found to block bacterial co-aggregation and biofilm formation.[88] Beyond berries, anthocyanin-rich extracts from black rice (anthocyanin 3-O-glucoside rich extract) [Supplementary Figure 7], suppressed CagA and VacA expression while protecting host cells,[89] pomegranate peel extracts (rich in delphinidin-3-O-glucoside) enhanced metronidazole efficacy and reduced inflammation,[90] and Solanum nigrescens anthocyanin fraction [rich in delphinidin-3-(p-coumaroyl)-rutinoside-5-glucoside] inhibited H. pylori via non-competitive urease inhibition.[91] Collectively, anthocyanins act primarily by reducing adhesion and biofilm formation, but also through suppression of virulence factors, urease inhibition, and modulation of inflammation, underscoring their potential as safe natural agents against H. pylori.

Supplementary Figure 7

Tannins: Tannoids (or tannins) are naturally occurring plant-derived polyphenolic compounds capable of binding and precipitating proteins, amino acids, and alkaloids, and they are widely recognised as promising antimicrobial agents.[92] Several studies have reported their in vitro activity against H. pylori.[93,94] Funatogawa et al. (2004) demonstrated that monomeric hydrolyzable tannoids, such as tellimagrandin I and II [Supplementary Figure 7], exert strong antibacterial effects by disrupting the bacterial membrane of H. pylori.[95] Beyond their antimicrobial role, tannoids also display anti-inflammatory properties by lowering nitric oxide levels and protecting the gastric mucosa from inflammation-associated damage.[96]

3.4. Clinical trials

Several natural products have been evaluated in clinical studies for their effects on H. pylori infection, with varying degrees of success [Table 1]. Broccoli sprouts, rich in sulforaphane, demonstrated moderate eradication rates when used alone and significantly enhanced outcomes when combined with standard triple therapy. Curcumin, although ineffective in significantly eradicating H. pylori on its own, consistently improved gastrointestinal symptoms and oxidative stress markers, making it a valuable adjunct. Nigella sativa showed eradication rates comparable to standard therapy at specific doses, while also relieving dyspeptic symptoms. Licorice root extract was one of the few natural products effective as monotherapy, achieving a 56% eradication rate, and it also proved beneficial when used with conventional therapy. Other botanicals, such as combinations like garlic with capsaicin, showed limited or inconsistent efficacy, though some improved inflammatory or oxidative stress markers. Overall, while most natural products do not achieve eradication rates sufficient to replace antibiotics, especially when used in conjunction with conventional therapies enhance eradication efficacy, reduce inflammation, and improve patient symptoms.[96]

Table 1: Clinical Trials on Medicinal Plants with H. pylori activity.[96]
Intervention Sample size Dose and treatment duration Outcome
Broccoli Sprouts 86 6 g/day broccoli sprout powder alone or with triple therapy Eradication: 56% (alone), 91.7% (with triple therapy)
Broccoli Sprout extract 89 250 mg extract contains 1000 g sulforaphane twice daily No significant eradication, reduced oxidative stress
Curcumin (30 mg) 25 Curcumin + bovine lactoferrin + N-acetylcysteine + pantoprazole 12% eradication, symptom improvement
Curcumin (500 mg) 60 Curcumin + triple therapy Eradication higher than placebo; better symptom relief
Curcumin + triple therapy 100 Triple therapy + 700 mg turmeric TID for 28 days Improved oxidative stress markers
Garlic Powder 36 2 g/day for 8 weeks 87% negative Urea Breath Test (UBT) vs. 73% placebo (not significant)
Garlic Oil 20 4 mg 4x/day for 14 days No improvement in symptoms or eradication
Garlic and Capsaicin 12 Garlic or capsaicin with meals No beneficial effect on H. pylori
Licorice extract 107 150 mg/day for 60 days Eradication: 56% vs. 4% (placebo)
Nigella sativa + Omeprazole 88 1-3 g/day + 40 mg omeprazole 66.7% eradication (2 g dose), similar symptom relief
Licorice + Probiotic 142 Fermented milk with 100 mg licorice + Lactobacillus paracasei Improved symptoms, UBT, inflammation
Licorice + triple therapy 120 Triple therapy + 380 mg licorice BID Eradication: 83.3% vs. 62.5% (control)
Nigella sativa honey formulation 70 5 mL/day + anti-secretory agent Improved dyspepsia and infection rate
Mastic gum 52 350 mg or 1 g TID, with/without pantoprazole Eradication: 38% in some groups, less than standard therapy

TID: Three times a day, BID: Twice a day

4. CONCLUSION

H. pylori remains a major global health concern, not only because of how widespread it is, but also due to its strong links to stomach cancer and growing resistance to standard antibiotics. This has sparked interest in the use of natural products; especially plant-based compounds; as potential allies in the fight against this stubborn bacterium. Many plant extracts, including those rich in alkaloids, flavonoids, terpenoids, tannins, and essential oils, show promising multi-targeted activity against H. pylori. These natural compounds can block the bacterium’s urease enzyme, prevent it from sticking to stomach cells, disrupt its cell membrane, and reduce the expression of harmful proteins like CagA and VacA. They also help regulate inflammation in the stomach lining. Even better, several of these compounds seem to work synergistically with antibiotics, potentially boosting treatment success and helping to tackle antibiotic resistance. Early clinical studies on natural products like Nigella sativa (black seed), licorice, broccoli sprouts, and curcumin show that they may enhance eradication rates, reduce oxidative stress, and ease digestive symptoms; especially when combined with standard treatments. However, most of these natural remedies aren’t effective enough to be used on their own just yet.

To move forward, we need more well-designed clinical trials to validate the benefits of these plant-based compounds. It’s also important to better understand how they work in the body, determine the best doses, and ensure long-term safety. Innovations in drug delivery, such as nanoparticles, encapsulation, or herbal blends might improve the way these compounds are absorbed and utilised. Additionally, advanced tools like systems biology and computer modelling can speed up the discovery of new plant-based therapies and uncover how they target multiple aspects of H. pylori infection.

In the long run, bridging the gap between laboratory research and clinical evidence will be essential to making phytotherapy a trusted part of H. pylori treatment, either as a supportive addition or a future alternative to traditional antibiotics.

4.1. Technological implications and interdisciplinary relevance

The integration of modern technology has greatly strengthened the therapeutic potential of natural products against Helicobacter pylori. Advanced analytical tools such as Ultra-Performance Liquid Chromatography–Quadrupole Time-of-Flight Mass Spectrometry (UPLC-QTOF-MS), Liquid Chromatography–Tandem Mass Spectrometry (LC-MS/MS), and Nuclear Magnetic Resonance (NMR) enable precise identification and structural elucidation of bioactive phytochemicals, accelerating the discovery of anti-H. pylori agents. Computational approaches, including molecular docking, molecular dynamics, and artificial intelligence, further enhance this process by predicting interactions with key bacterial targets such as urease, CagA, and VacA, while network pharmacology clarifies their multi-target effects. Nanotechnology contributes by improving the bioavailability and stability of natural compounds through nanoparticles, encapsulation, and targeted delivery systems, thereby overcoming limitations of poor solubility or degradation in the gastric environment. Finally, clinical translation is supported by advanced diagnostic tools such as the urea breath test (UBT) and molecular assays, coupled with rigourously designed clinical trials that validate efficacy and safety. Collectively, these technological advancements create a powerful platform to transform natural products into effective adjunct therapies, offering multi-targeted strategies to combat antibiotic-resistant H. pylori.

4.2. Future directions

Future research on natural products for H. pylori should focus on conducting rigourous clinical trials, standardising extract quality, and studying safety and pharmacokinetics. Combining these compounds with antibiotics or probiotics could improve treatment outcomes, especially when delivered via advanced technologies like nanoparticles. Efforts should also target biofilm disruption and resistance mechanisms. Tools like systems biology and computational modelling can accelerate discovery, while personalised strategies may enhance effectiveness based on individual host and microbiome profiles.

Ethical approval

Institutional Review Board approval is not required.

Declaration of patient consent

Patient’s consent not required as there are no patients in this study.

Financial support and sponsorship

Nil

Conflicts of interest

There are no conflicts of interest.

Use of artificial intelligence (AI)-assisted technology for manuscript preparation

The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript and no images were manipulated using AI.

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