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Metabolites
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Flavonoids: Novel Therapeutic Potential for Chronic Diseases
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Flavonoids: Novel Therapeutic Potential for Chronic Diseases

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Endocrinology and Clinical Metabolic Research".

Deadline for manuscript submissions: 31 October 2025 | Viewed by 676

Special Issue Editors

Dr. Aleksandra Kozłowska

E-Mail Website
Guest Editor
Department of Social Medicine and Public Health, Medical University of Warsaw, 02-106 Warsaw, Poland
Interests: flavonoids; antioxidants; antioxidant activity; diabetes; inflammation; preventive medicine; oxidative stress biomarkers; human diet; pregnancy
Prof. Dr. Shawn R. Campagna

E-Mail Website
Guest Editor
Department of Chemistry, University of Tennessee, Knoxville, TN 37996, USA
Interests: metabolomics; lipidomics; chemical biology; environmental, animal, and human health; metabolism

Special Issue Information

Dear Colleagues,

Flavonoids are a group of bioactive compounds widely found in plant-based foodstuffs known for their antioxidant, anti-inflammatory, and anti-carcinogenic properties. At the molecular level, their actions include antioxidant effects and the ability to modulate several key enzymatic pathways. The growing body of scientific evidence indicates that flavonoids play a beneficial role in disease management and prevention of chronic diseases such as cardiovascular disorders, diabetes, cancer, and neurodegenerative conditions. However, there is an urgent need for further clinical and epidemiological trials.

This Special Issue aims to explore the latest research on flavonoids’ molecular mechanisms, bioavailability, and clinical applications in chronic disease treatment. We invite original research articles and reviews that address topics such as flavonoid metabolism, their interaction with cellular pathways, and their role in modulating oxidative stress, inflammation, and immune responses. Additionally, we encourage studies examining the synergistic effects of flavonoids with other bioactive compounds, as well as their therapeutic potential.

The goal of this Special Issue is to provide a comprehensive overview of flavonoids’ role in chronic disease management, offering insights into their future applications in therapeutic interventions.

Dr. Aleksandra Kozłowska
Prof. Dr. Shawn R. Campagna
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Metabolites is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • flavonoids
  • chronic diseases
  • inflammation
  • diabetes
  • anthocyanins
  • cardiovascular diseases
  • neurodegenerative disorders
  • quercetin

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Published Papers (2 papers)

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Research

15 pages, 1611 KiB  
Article
Angiotensin-Converting Enzyme Inhibitory Activity of Selected Phenolic Acids, Flavonoids, Their O-Glucosides, and Low-Molecular-Weight Phenolic Metabolites in Relation to Their Oxidation Potentials
by Danuta Zielińska, Małgorzata Starowicz, Małgorzata Wronkowska and Henryk Zieliński
Metabolites 2025, 15(7), 443; https://doi.org/10.3390/metabo15070443 - 1 Jul 2025
Viewed by 194
Abstract
Background/Objectives: In this study, the angiotensin-converting enzyme (ACE) inhibitory activity of selected phenolic acids, flavonoids, their O-glucosides, and low-molecular-weight phenolic metabolites was addressed to show their importance against blood hypertension. Methods: A fluorescence assay was used for the determination of [...] Read more.
Background/Objectives: In this study, the angiotensin-converting enzyme (ACE) inhibitory activity of selected phenolic acids, flavonoids, their O-glucosides, and low-molecular-weight phenolic metabolites was addressed to show their importance against blood hypertension. Methods: A fluorescence assay was used for the determination of the ACE inhibitory activity, whereas the first anodic peak oxidation potential (Epa) was provided by the differential pulse voltammetry (DPV) method. The relationship between the ACE inhibitory activity and Epa was evaluated. Results: Phenolic acids showed a very low ACE inhibitory activity, and their rank was chlorogenic acid > p-coumaric acid > sinapic acid > gentisic acid > ferulic acid > syringic acid > vanillic acid > protocatechuic acid > caffeic acid. The low-molecular-weight phenolic metabolites of flavonoids showed a moderate ACE inhibitory activity. In contrast, flavonoid aglicones had the highest ACE inhibitory activity, and the order was luteolin > quercetin > kaempferol > cyanidin > delphinidin > pelargonin > naringenin. A lower inhibition activity was noted for quercetin-3-O-glucoside, luteolin-4′-O-glucosides, cyanidin-3-O-glucoside, and pelargonidin-3-O-glucosides, whereas a higher ACE inhibition activity was observed for 7-O-glucosides of luteolin, apigenin, and kaempferol. A lack of correlation was found between the IC50 of phenolic acids, low-molecular-weight phenolic metabolites, and their Epa values. In contrast, weak positive correlations were found between the IC50 of aglicons, 3-O-glucosides, 7-O-glucosides, and their Epa values provided by the DPV (r = 0.61, r = 0.66 and r = 0.88, respectively). Conclusions: This study expands our knowledge of the ACE inhibitory activity of phenolic compounds. Full article
(This article belongs to the Special Issue Flavonoids: Novel Therapeutic Potential for Chronic Diseases)
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18 pages, 3098 KiB  
Article
(-)-Epigallocatechin-3-Gallate Suppresses Hyperexcitability in Rat Primary Nociceptive Neurons Innervating Inflamed Tissues: A Comparison with Lidocaine
by Syogo Utugi, Yukito Sashide and Mamoru Takeda
Metabolites 2025, 15(7), 439; https://doi.org/10.3390/metabo15070439 - 1 Jul 2025
Viewed by 242
Abstract
Objective: Given the side effects and reduced efficacy of conventional local anesthetics in inflammatory conditions, there is a compelling need for complementary alternative medicine (CAM), particularly those based on phytochemicals. While a previous study showed that in vivo local injection of (-)-epigallocatechin-3-gallate (EGCG) [...] Read more.
Objective: Given the side effects and reduced efficacy of conventional local anesthetics in inflammatory conditions, there is a compelling need for complementary alternative medicine (CAM), particularly those based on phytochemicals. While a previous study showed that in vivo local injection of (-)-epigallocatechin-3-gallate (EGCG) into the peripheral receptive field suppresses the excitability of rat trigeminal ganglion (TG) neurons in the absence of inflammation, the acute effects of EGCG in vivo, especially on TG neurons under inflammatory conditions, are still unknown. We aimed to determine if acute local EGCG administration into inflamed tissue effectively attenuates the excitability of nociceptive TG neurons evoked by mechanical stimulation. Methods: The escape reflex threshold was measured to assess hyperalgesia caused by complete Freund’s adjuvant (CFA)-induced inflammation. To assess neuronal activity, extracellular single-unit recordings were performed on TG neurons in anesthetized CFA-inflamed rats in response to orofacial mechanical stimulation. Results: The mechanical escape threshold was significantly lower in CFA-inflamed rats compared to before CFA injection. EGCG (1–10 mM) reversibly and dose-dependently inhibited the mean firing frequency of TG neurons evoked by both non-noxious and noxious mechanical stimuli (p < 0.05). For comparison, 1% lidocaine (37 mM), a local anesthetic, also caused reversible inhibition of the mean firing frequency in inflamed TG neurons responding to mechanical stimuli. Importantly, 10 mM EGCG produced a significantly greater magnitude of inhibition on TG neuronal discharge frequency than 1% lidocaine (noxious, lidocaine vs. EGCG, 19.7 ± 3.3% vs. 42.3 ± 3.4%, p < 0.05). Conclusions: Local injection of EGCG into inflamed tissue effectively suppresses the excitability of nociceptive primary sensory TG neurons, as indicated by these findings. Significantly, locally administered EGCG exerted a more potent local analgesic action compared to conventional voltage-gated sodium channel blockers. This heightened efficacy originates from EGCG’s ability to inhibit both generator potentials and action potentials directly at nociceptive primary nerve terminals. As a result, EGCG stands out as a compelling candidate for novel analgesic development, holding particular relevance for CAM strategies. Full article
(This article belongs to the Special Issue Flavonoids: Novel Therapeutic Potential for Chronic Diseases)
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