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Advances in Phytochemical Research: Molecular Pathways in Health and Disease

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A Special Issue of Current Issues in Molecular Biology (ISSN 1467-3045) belonging to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (31 May 2026) | Viewed by 14048

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Dr. Christiana Charalambous

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Department of Basic and Clinical Sciences, University of Nicosia Medical School, 1683 Nicosia, Cyprus
Interests: breast cancer; natural compounds; phytochemicals; estrogen receptors; tamoxifen resistance; chemoprevention
Special Issues, Collections and Topics in MDPI journals

Dr. Christiana M. Neophytou

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Apoptosis and Cancer Chemoresistance Laboratory, Basic and Translational Cancer Research Center, Department of Life Sciences, European University Cyprus, 2404 Nicosia, Cyprus
Interests: cancer biology; targeted cancer therapy; apoptosis; metastasis; cancer chemoresistance; pancreatic cancer; breast cancer; lung cancer
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Bioactive phytochemicals, including flavonoids, alkaloids, and terpenoids, have been reported to regulate cellular processes such as inflammation, oxidative stress, and apoptosis. Based on these mechanisms, we can develop new therapeutic strategies for diseases such as cancer, cardiovascular disorders, and metabolic syndromes, promoting the use of natural products in preventive and therapeutic medicine. Clinical trials and epidemiological studies continue to support the notion that a diet rich in phytochemicals correlates with improved health outcomes and may help prevent various diseases. Importantly, recent advancements in bioinformatics and molecular biology techniques have led to a better understand of the mechanisms through which these phytochemicals exert their effects. By studying specific molecular pathways, such as NF-kB and MAPK signaling, we can uncover how phytochemicals can modulate gene expression and protein function. Therefore, the aim of this Special Issue is to provide an overview of advances in phytochemical research by exploring how plant-derived compounds affect molecular pathways implicated in health and disease.

For this collection, we invite submissions on the following topics:

Isolation and characterization of phytochemicals with potential medicinal properties.
Anti-oxidant properties of phytochemicals and their role in combating oxidative stress.
Anti-inflammatory effects and the modulation of immune responses.
Phytochemicals’ effect on cell signaling pathways (e.g., NF-kB, MAPK, apoptosis signaling).
The role of phytochemicals in cancer prevention and treatment.
Impacts on cardiovascular health and metabolic syndromes.
Neuroprotective effects of phytochemicals in neurodegenerative diseases.
The development of phytochemical-based drugs and nutraceuticals.
Synergistic effects of phytochemicals with conventional therapies.
Research on phytochemicals in clinical trials.
Genetic and epigenetic regulation by phytochemicals.
Interactions between phytochemicals and gut microbiota.
Advances in methodologies for studying phytochemicals (e.g., metabolomics, transcriptomics).
Potential for developing precision medicine approaches using phytochemicals.
Explorations of traditional medicinal plants and their phytochemical constituents.

These topics collectively contribute to a deeper understanding of how phytochemicals influence health outcomes and provide insights into potential therapeutic applications in the context of various diseases.

Dr. Christiana Charalambous
Dr. Christiana Neophytou
Guest Editors

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Current Issues in Molecular Biology is an international peer-reviewed open access monthly journal published by MDPI.

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Keywords

phytochemicals
molecular mechanisms
cancer signaling pathways
anti-inflammatory properties
anti-oxidant properties
apoptosis
cardiovascular disorders
metabolic syndromes
chemoprevention

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Published Papers (10 papers)

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Research

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10 pages, 2498 KB

Open AccessArticle

Benincaside A Induces p53-Dependent Transactivation and Fas/CD95-Mediated Apoptosis in HCT 116 Human Colorectal Cancer Cells

by Jai-Sing Yang, Kun-Ching Cheng, Yu-Hsiu Chuang, Ping-Chung Kuo and Tian-Shung Wu

Curr. Issues Mol. Biol. 2026, 48(6), 635; https://doi.org/10.3390/cimb48060635 - 18 Jun 2026

Viewed by 408

Abstract

An undescribed seco-kaurane diterpenoid, benincaside A (BA), was isolated from the seeds of Benincasa hispida. The seeds of B. hispida have been traditionally used in folk medicine and previous studies have reported anti-tumor potential in B. hispida seed extracts. Accordingly, we investigated the cytotoxicity and underlying mechanisms of BA in colorectal cancer cells. BA inhibited growth in HT29, Colo205, HCT116, and CT26 colorectal cancer cells, as determined by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, while showing no toxicity toward normal human umbilical vein endothelial cells (HUVEC) and human fibroblast WS-1 cells. In HCT116 cells, BA-induced deoxyribonucleic acid (DNA) damage and apoptosis, as evidenced by morphological changes, 4,6-diamidino-2-phenylindole dihydrochloride (DAPI) staining, and assays of caspase-8 and caspase-3 activities. BA triggered apoptotic cell death via the extrinsic pathway, as indicated by elevated caspase-8 and caspase-3 activities. Intracellular reactive oxygen species (ROS) generation was observed in BA-treated HCT116 cells. The growth-inhibitory effects were significantly attenuated by pretreatment with N-acetylcysteine (NAC, an antioxidant), caffeine (an ATM kinase inhibitor), z-VAD-fmk (pan-caspase inhibitor), or z-IETD-fmk (caspase-8-specific inhibitor). Colorimetric assays confirmed increased caspase-8 and caspase-3 activities in BA-treated cells. This study is the first to report ROS-dependent signaling as a key mechanism underlying BA-induced cell death in HCT116 human colorectal cancer cells. Full article

(This article belongs to the Special Issue Advances in Phytochemical Research: Molecular Pathways in Health and Disease)

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25 pages, 3645 KB

Open AccessArticle

Temporal Effects of Cigarette Smoke and Phytochemical-Based E-Liquid Aerosols on Tracheo-Alveolar Histopathology and the IL-6/TNF-α Molecular Signaling Axis

by Awal Prasetyo, Dora Maftikhati, Levina Athaya Anarizta, Nazhira Ghina Setyawan, Anindha Waradita Putri Yuwono, Maria Meutia Saleha, Farahdita Ramadhanti Annisa Mukti, Hermawan Istiadi, Udadi Sadhana and Fathur Nur Kholis

Curr. Issues Mol. Biol. 2026, 48(6), 618; https://doi.org/10.3390/cimb48060618 - 15 Jun 2026

Cited by 1 | Viewed by 508

Abstract

This study compared the temporal effects of traditional cigarettes and e-cigarettes on lung health in male Rattus norvegicus over 8- and 12-week periods. Thirty rats were evaluated for tracheal/alveolar histopathology and systemic markers (IL-6, TNF-α, SOD-3, MDA). Chronic cigarette exposure (12 weeks) and nicotine aerosol (8 weeks) significantly suppressed weight gain, while ascorbic acid aerosol caused less growth inhibition. At 8 weeks, cigarette exposure (K3) induced adaptive tracheal mucosal thickening (66.88 ± 17.92 µm vs. 52.40 ± 2.63 µm in control K1), increased goblet cells (4.2 ± 2.44 N/mm), elevated SOD-3 (12.75 ± 1.10 pg/mL), and initiated emphysematous alveolar expansion (469.77 ± 91.31 µm vs. 202.03 ± 29.38 µm in K1 in K1). Conversely, 12-week cigarette smoke (K4) triggered epithelial exhaustion, significantly thinning the tracheal mucosa (34.65 ± 6.55 µm) and elevating systemic IL-6 (11.45 ± 1.17 pg/mL vs. 8.43 ± 0.88 pg/mL in control K2). Notably, chronic electronic ascorbic acid aerosolization (K6) preserved localized alveolar structural layouts and limited septal thickening compared with nicotine groups. However, it failed to suppress systemic inflammation, as evidenced by elevated IL-6 levels. In conclusion, while ascorbic acid aerosols moderate localized parenchymal destruction compared to nicotine, chronic aerosol exposure accelerates systemic immune activation. Full article

(This article belongs to the Special Issue Advances in Phytochemical Research: Molecular Pathways in Health and Disease)

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27 pages, 2295 KB

Open AccessArticle

Phytochemical Analysis, GC-MS Chemical Profiling, and In Vitro Antidiabetic Evaluation of South African Momordica balsamina Linn Leaf Extracts and Its Effects on Oxidative Stress Modulation

by Buang Matseke, Daniel Tswaledi and Kokoette Bassey

Curr. Issues Mol. Biol. 2026, 48(5), 503; https://doi.org/10.3390/cimb48050503 - 13 May 2026

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Abstract

Background: Momordica balsamina L. is widely used in traditional medicine for the management of diabetes in South Africa and globally. This study evaluated the in vitro antidiabetic and cytotoxic effects of M. balsamina leaf extracts and identified bioactive compounds potentially responsible for its activity. Methods: Leaves were sequentially extracted using solvents of increasing polarity. Phytochemical composition was determined using standard colorimetric assays, while gas chromatography–mass spectrometry (GC–MS) was employed for compound identification. Antioxidant activity was evaluated using dot blot, DPPH radical scavenging, hydrogen peroxide scavenging, and ferric reducing power assays. Antidiabetic potential was assessed using α-amylase, α-glucosidase, and β-glucosidase inhibitory assays, with acarbose as the reference drug. Cytotoxicity was determined by using the MTT assay on Vero and HEK-293 cell lines. Results: Phytochemical screening revealed alkaloids, flavonoids, terpenoids, saponins, glycosides, and steroids. GC–MS analysis identified compounds associated with antidiabetic activity, including vanillin, 2,4-di-tert-butylphenol, oleic acid, phytol, and hexadecenoic acid. All extracts exhibited antioxidant activity, with the ethyl acetate extract showing the strongest effect. Enzyme inhibition was concentration dependent. The dichloromethane and ethyl acetate extracts showed stronger α-amylase inhibition (IC₅₀ = 0.149 and 0.146 mg/mL) than acarbose (0.209 mg/mL). For α-glucosidase, acarbose showed the highest activity, while extracts displayed moderate inhibition. In β-glucosidase assays, both extracts were more active than acarbose. Both extracts were non-cytotoxic up to 500 µg/mL. Conclusions: These findings support the traditional use of M. balsamina and highlight its potential as a safe source of antidiabetic agents, warranting further investigation. Full article

(This article belongs to the Special Issue Advances in Phytochemical Research: Molecular Pathways in Health and Disease)

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21 pages, 8614 KB

Open AccessArticle

Eupatorium lindleyanum DC. Suppresses Cytokine Storm by Inhibiting NF-κB and PI3K–Akt Signaling in Sepsis-Associated and Virus-Related Acute Lung Injury

by Chen Luo, Peilin He, Yan Yang, Lian Xia, Wenjie Xu, Daike Zou, Yiduo Feng, Lian Duan, Junjie Deng, Yong Jing and Xianqin Luo

Curr. Issues Mol. Biol. 2026, 48(3), 333; https://doi.org/10.3390/cimb48030333 - 21 Mar 2026

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Abstract

Cytokine storm is a central pathogenic mechanism underlying sepsis-induced acute lung injury (SALI) and severe coronavirus disease 2019 (COVID-19), yet effective therapeutic strategies remain limited. Eupatorium lindleyanum DC. (EL), a traditional Chinese medicinal herb, has been reported to possess anti-inflammatory, antioxidant, and antiviral-related activities; however, its protective mechanisms in SALI and virus-associated inflammatory lung injury remain incompletely understood. In this study, an integrated strategy combining computational prediction and experimental validation was employed to investigate the therapeutic potential and underlying mechanisms of EL. The chemical constituents of EL were characterized by UPLC–Q–TOF/MS, followed by network pharmacology, molecular docking, and molecular dynamics analyses to predict key targets and signaling pathways. A cecal ligation and puncture (CLP)-induced SALI rat model was used to evaluate lung histopathology, pulmonary edema, cytokine production, and inflammatory signaling activation. In parallel, LPS-stimulated RAW264.7 macrophages were used to assess cytokine secretion and pathway regulation in vitro. In addition, a SARS-CoV-2 pseudovirus-induced mouse model was employed to further evaluate the in vivo relevance of the representative bioactive compound hyperoside in pseudovirus-associated lung injury. A total of 32 active compounds and 697 putative targets were identified, among which 116 were associated with sepsis and COVID-19. In vivo, EL markedly alleviated lung injury, reduced the lung coefficient and wet/dry ratio, and suppressed excessive production of proinflammatory cytokines and activation of key signaling proteins. In vitro, EL dose-dependently inhibited TNF-α and IL-6 secretion and regulated the PI3K–Akt and NF-κB signaling pathways. Notably, hyperoside showed favorable predicted interactions with PI3K–Akt pathway-related targets (EGFR, PI3K, and Akt), while molecular dynamics simulations supported stable interactions with several COVID-19-related targets, including ACE2, Mpro, and RdRp. Furthermore, hyperoside significantly alleviated SARS-CoV-2 pseudovirus-associated lung injury, reduced ACE2 protein expression, and downregulated EGFR, PI3K, and Akt mRNA levels in vivo. Collectively, these findings indicate that EL exerts protective effects through multi-component, multi-target, and multi-pathway mechanisms, and support its potential value for further investigation in SALI and virus-associated inflammatory lung injury. Full article

(This article belongs to the Special Issue Advances in Phytochemical Research: Molecular Pathways in Health and Disease)

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17 pages, 7114 KB

Open AccessArticle

A Water Extract of Mixed Mushroom Mycelia Mitigates Cognitive Deficit and Oxidative Stress After Global Cerebral Ischemia–Reperfusion Injury

by Hyeon-Jeong Noh, Ji-Hyun Moon, Hye Jeong Ahn, Ah La Choi, Nam Seob Lee, Young Gil Jeong, Sang Seop Lee, Yung Choon Yoo, Ji-Min Lee, Do-Eun Kim, Jaeku Kang, Jong Yea Park, Hyun Min Kim, Sung Baek Kim and Seung Yun Han

Curr. Issues Mol. Biol. 2026, 48(2), 151; https://doi.org/10.3390/cimb48020151 - 29 Jan 2026

Viewed by 934

Abstract

Background: GMK is a bioactive material newly identified from a water extract of mixed mushroom mycelia (Phellinus linteus, Inonotus obliquus, and Ganoderma lucidum). It has shown protective effects against glutamate-induced excitotoxicity and lipopolysaccharide-triggered neuroinflammation. However, whether GMK can ameliorate global cerebral ischemia–reperfusion injury (GCIRI) and its associated cognitive deficit remains to be elucidated. Methods: GCIRI was induced in male Sprague–Dawley rats by bilateral common carotid artery occlusion with hypovolemia (BCCAO/H). GMK (30 or 90 mg/kg, p.o.) was administered once daily for 14 days before surgery. Cognitive functions were evaluated using the Y-maze, Barnes maze, and passive avoidance tests. Hippocampal CA1 neuronal survival and glial activation were analyzed by cresyl violet staining and Iba1/GFAP immunohistochemistry. In parallel, PC12 cells were pretreated with GMK (100 or 200 μg/mL, 24 h) before oxygen–glucose deprivation and reoxygenation (OGD/R), and apoptosis (TUNEL, Bax/Bcl-2), oxidative stress markers (ROS, MDA, and NO), antioxidant enzymes including glutathione peroxidase (GPX) and catalase (CAT), and signaling proteins (p-ERK/ERK, iNOS) were examined. Results: GMK significantly ameliorated GCIRI-induced learning and memory impairments, protected CA1 pyramidal neurons, and reduced microglial and astrocytic activation. In OGD/R-challenged PC12 cells, GMK attenuated apoptosis, suppressed ROS, MDA, and NO production, normalized GPX and CAT activities, and favorably regulated p-ERK and iNOS pathways. Conclusions: These findings suggest that GMK confers dose-dependent behavioral and histopathological protection against GCIRI, potentially by modulating redox- and apoptosis-related signaling (Bax/Bcl-2, GPX/CAT, and ERK/iNOS pathways), with more consistent effects at a higher dose. Full article

(This article belongs to the Special Issue Advances in Phytochemical Research: Molecular Pathways in Health and Disease)

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15 pages, 934 KB

Open AccessArticle

Lycopene Mitigates Rat Liver Damage Induced by Lipopolysaccharide via Mechanisms Involving Oxidative Stress, Inflammation, and Apoptosis

by Snežana Tešić Rajković, Andrija Rančić, Marko Stojanović, Jelena Živadinović, Ivana Ramić, Milica Nestorović, Sava Spasić, Elena Stanković, Ivan Nagorni, Vesna Brzački, Ilija Ilić, Miloš Dičić and Dušan Sokolović

Curr. Issues Mol. Biol. 2025, 47(11), 914; https://doi.org/10.3390/cimb47110914 - 4 Nov 2025

Cited by 2 | Viewed by 1281

Abstract

Background: Sepsis is a leading cause of mortality in intensive care units, with liver dysfunction representing a critical determinant of poor outcome, mainly associated with excessive inflammation and oxidative stress. Lycopene, a carotenoid with potent antioxidant and anti-inflammatory properties, has been proposed as a potential therapeutic agent. This study investigated whether lycopene supplementation mitigates lipopolysaccharide-induced oxidative and inflammatory liver injury in rats. Methods: Male Wistar rats, divided into four groups, were exposed to either lipopolysaccharide or a combination of lipopolysaccharide (10 mg/kg) and lycopene (6 mg/kg). In order to assess liver damage induced by lipopolysaccharide, hepatocellular injury markers, oxidative stress indices, nitric oxide metabolism, glutathione redox status, apoptotic enzyme activity, and inflammatory mediators were assessed in serum and liver tissue. Results: Lipopolysaccharide induced marked hepatocellular damage, characterized by elevated serum liver-cell damage parameters, and liver tissue xanthine oxidase, myeloperoxidase, thiobrabituric reactive substances, protein carbonyl content, deoxyribonuclease I/II activity, nuclear factor kappa B, tumor necrosis factor-α, and interleukin-6, alongside depletion of reduced glutathione and reduced glutathione reductase and glutathione peroxidase activities. Lyc pretreatment significantly attenuated liver enzyme leakage, oxidative damage, and cytokine release while restoring reduced glutathione and glutathione reductase activity. In contrast, lycopene had limited effects on glutathione peroxidase activity, nitric oxide/inducible nitric oxide synthase signaling, and nuclear factor erythroid 2-related factor 2 expression. Conclusions: These findings demonstrate that lycopene confers partial hepatoprotection in endotoxemic rats, primarily through suppression of oxidative damage and nuclear factor kappa B-mediated inflammation. Further studies are needed to clarify tissue-specific mechanisms and optimize dosing strategies in order to increase the efficacy of this carotenoid. Full article

(This article belongs to the Special Issue Advances in Phytochemical Research: Molecular Pathways in Health and Disease)

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17 pages, 2436 KB

Open AccessArticle

Salvianolic Acid B Attenuates Liver Fibrosis via Suppression of Glycolysis-Dependent m1 Macrophage Polarization

by Hao Song, Ze-Wei Li, Wei Xu, Yang Tan, Ming Kuang, Gang Pei and Zhi-Qi Wang

Curr. Issues Mol. Biol. 2025, 47(8), 598; https://doi.org/10.3390/cimb47080598 - 29 Jul 2025

Cited by 4 | Viewed by 2504

Abstract

Liver fibrosis, a critical pathological feature of chronic liver injury, is closely associated with macrophage-mediated inflammatory responses and metabolic reprogramming. Blocking the fibrosis process will be beneficial to the treatment and recovery of the disease. Liver macrophages are a remarkably heterogeneous population of immune cells that play multiple functions in homeostasis and are central to liver fibrosis. Glycolysis-mediated macrophage metabolic reprogramming leads to an increase in the proportion of M1 macrophages and the release of pro-inflammatory cytokines. The present study aimed to investigate the therapeutic effect and mechanism of acid B (SAL B) against carbon tetrachloride (CCl₄)-induced liver fibrosis. Here, we demonstrate that SAL B reduced the production of inflammatory factors in CCl₄-induced liver fibrosis. Mechanistically, SAL B increased the expression of migration inhibitor 1 (MIG1) by inhibiting DNMT1-mediated methylation of the MIG1 promoter. Subsequently, MIG1 reduced the transcription of lactate dehydrogenase A (LDHA) and hexokinase 2 (HK2) which blocked glycolysis-mediated macrophage M1 polarization. In summary, our results suggested that SAL B is a promising intervention for ameliorating liver fibrosis. Full article

(This article belongs to the Special Issue Advances in Phytochemical Research: Molecular Pathways in Health and Disease)

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Review

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40 pages, 2025 KB

Open AccessReview

Natural Plant-Derived Compounds Targeting Oxidative Stress and Inflammation in NAFLD—Mechanisms and Repositioning Potential

by Rafailia-Eirini Theodorou, Nikiforos Vrettos and Panagiotis Theodosis-Nobelos

Curr. Issues Mol. Biol. 2026, 48(5), 465; https://doi.org/10.3390/cimb48050465 - 29 Apr 2026

Cited by 1 | Viewed by 613

Abstract

Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease, with advanced stages potentially progressing to hepatocellular carcinoma. It is a multifactorial condition associated with metabolic syndrome, diabetes, and hormonal imbalance, leading to metabolic alterations that are intensified by inflammation. An important additional factor that amplifies these effects is oxidative stress, which interacts with inflammatory pathways and contributes to disease progression. This review evaluates evidence from in vitro, in vivo, and clinical studies on widely investigated natural compounds, including cinnamic acid, stilbene and quinone derivatives, coumarinoids, tannins, and miscellaneous phenol-containing compounds and alkaloids, focusing on their antioxidant, anti-inflammatory and multi-functional properties. These compounds have demonstrated beneficial effects such as reduction of lipid accumulation, improvement of insulin resistance, modulation of inflammatory cytokines (e.g., TNF-α, IL-6), and attenuation of oxidative stress markers, with several studies reporting improvements in liver enzymes and histological features of steatosis. The aim is to assess their potential to improve NAFLD beyond their established biological activities and to explore their repositioning potential as multi-targeted agents for complementary or second-line therapeutic strategies. Their plant-derived origin and broad therapeutic profiles suggest a favorable safety margin. However, further well-designed clinical studies are required to better define their efficacy, optimal dosing, pharmacokinetics and safety, as well as to clarify their mechanisms of action and their potential role in NAFLD management. Full article

(This article belongs to the Special Issue Advances in Phytochemical Research: Molecular Pathways in Health and Disease)

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45 pages, 1122 KB

Open AccessEditor’s ChoiceReview

Phytochemical Quorum-Sensing Inhibitors Against Bacterial Pathogens: Mechanisms of Action and Translational Challenges

by Christos Papaneophytou

Curr. Issues Mol. Biol. 2026, 48(2), 214; https://doi.org/10.3390/cimb48020214 - 14 Feb 2026

Cited by 16 | Viewed by 2426

Abstract

Antimicrobial resistance is a critical global health challenge, driven by the rapid emergence of multidrug-resistant bacterial pathogens and exacerbated by extensive antibiotic use, which imposes intense selective pressure and disrupts host-associated microbial communities. In this context, quorum sensing (QS), a conserved molecular communication system that coordinates population-level gene regulation, virulence expression, and biofilm development, has emerged as an attractive target for anti-virulence intervention. A growing body of evidence indicates that phytochemicals, such as curcumin, carvacrol, carnosol, eugenol, and chlorogenic acid, can modulate key QS pathways, including acyl-homoserine lactone-, autoinducing peptide-, and LuxS/AI-2-mediated signaling, thereby attenuating pathogenic behaviors at sub-inhibitory concentrations that do not directly impair bacterial viability. Despite this promise, the translational development of phytochemical-based QS inhibitors remains limited. Because QS also regulates cooperative and homeostatic functions in beneficial bacteria, QS-targeted interventions raise concerns about microbiome disruption and ecological imbalance. Furthermore, the literature is marked by substantial methodological heterogeneity, reliance on indirect phenotypic endpoints, limited molecular target validation, and insufficient assessment of toxicity, bioavailability, and pharmacokinetics. The predominance of simplified in vitro models further constrains extrapolation to complex host-associated and polymicrobial environments. This review critically examines the molecular mechanisms underlying phytochemical modulation of bacterial QS, synthesizes pathogen-focused experimental evidence, and evaluates key translational challenges arising from QS conservation, microbiome considerations, and methodological limitations. Addressing these barriers through mechanism-resolved experimentation, standardized evaluation frameworks, and microbiome-aware testing strategies will be essential for advancing phytochemical QS inhibitors toward clinically and industrially relevant anti-virulence applications. Full article

(This article belongs to the Special Issue Advances in Phytochemical Research: Molecular Pathways in Health and Disease)

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27 pages, 2804 KB

Open AccessReview

Phytochemical Composition and Mechanistic Pharmacology of Jerusalem Artichoke (Helianthus tuberosus L.): Implications for Functional and Therapeutic Applications

by Dong-Hwan Kim, Wonmin Lee, Yeonhee Pyo and Dong-Kug Choi

Curr. Issues Mol. Biol. 2026, 48(2), 180; https://doi.org/10.3390/cimb48020180 - 5 Feb 2026

Viewed by 2368

Abstract

Jerusalem artichoke (JA) (Helianthus tuberosus), a perennial plant of the Asteraceae family, is well known for its high inulin content and diverse bioactive compounds, including flavonoids, phenolic acids, sesquiterpenes, and amino acids. Extracts derived from different parts of JA, such as tubers, leaves, and flowers, have demonstrated a wide range of biological activities, including antioxidant, anti-inflammatory, antihyperglycemic, antihypertensive, and antifungal effects. These properties highlight JA’s potential in the prevention and management of chronic diseases such as diabetes, cardiovascular disorders, obesity, and colorectal cancer. Recent studies also suggest that JA benefits skin health through anti-aging and barrier-protective mechanisms and enhances immune function by modulating the intestinal microbiota. Owing to its multifunctional physiological activities, JA is being explored as a valuable raw material for food, nutraceutical, cosmetic, and pharmaceutical applications. However, most existing research has focused primarily on inulin, while comprehensive studies on other bioactive constituents and their clinical validation remain limited. This paper aims to provide a comprehensive overview of the bioactive compounds present in JA, elucidate their health-promoting functions, discuss their pharmacokinetics, and outline future perspectives on their potential as functional ingredients and biohealth materials. Full article

(This article belongs to the Special Issue Advances in Phytochemical Research: Molecular Pathways in Health and Disease)

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