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Harnessing Natural Bioactives for Sustainable Nutrition and Chronic Disease Control

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Dear Colleagues,

Natural bioactives, encompassing phytochemicals, microbial metabolites, and marine-derived compounds, represent a rich source of therapeutic agents with significant potential for drug discovery, health promotion, and chronic disease control. Their antioxidant, anti-inflammatory, and immunomodulatory properties show promise in modulating the progression of chronic diseases, including obesity, cardiovascular disorders, diabetes, and neurodegenerative conditions, although further large-scale clinical validation is warranted. Current research focuses on harnessing these compounds more effectively, advancing strategies such as nanoparticle-based delivery systems to enhance bioavailability and elucidating synergistic mechanisms of multicomponent interactions. Concurrently, ensuring the sustainable nutrition derived from these resources necessitates a critical balance between exploitation and ecological conservation. As a vital component of a "green pharmacopeia," natural bioactives offer a compelling foundation for shifting healthcare paradigms towards prevention-oriented strategies, providing innovative solutions for global public health challenges.

Dr. Lina Yang
Dr. Jihua Chen
Guest Editors

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11 pages, 1040 KB

Open AccessEditor’s ChoiceArticle

Functional Phytochemicals Cooperatively Suppress Inflammation in RAW264.7 Cells

by Kaori Terashita, Masato Kohakura, Katsura Sugawara, Shinichi Miyagawa and Gen-ichiro Arimura

Nutrients 2026, 18(3), 376; https://doi.org/10.3390/nu18030376 - 23 Jan 2026

Viewed by 7070

Abstract

Background: Chronic inflammation contributes to the development of lifestyle-related diseases, and dietary phytochemicals are recognized as important modulators of inflammatory responses. However, the synergistic anti-inflammatory effects of phytochemical combinations and their underlying mechanisms remain insufficiently understood. Methods: The anti-inflammatory activities of menthol (ME), 1,8-cineole (CI), β-eudesmol (EU), and capsaicin (CA) were evaluated in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages. Pro-inflammatory gene expression was quantified by quantitative PCR, intracellular Ca²⁺ signaling was assessed by calcium imaging, and the involvement of transient receptor potential (TRP) channels was examined using selective inhibitors. Synergistic effects were analyzed based on changes in half-maximal effective concentrations (EC₅₀). Results: All compounds suppressed LPS-induced pro-inflammatory genes, including tumor necrosis factor-alpha (Tnf) and interleukin-6 (Il6), in a dose-dependent manner, with CA showing the lowest EC₅₀ for Tnf expression (0.087 µM). Notably, combinations of CA with ME or CI exhibited strong synergy, reducing their EC₅₀ values by 699-fold and 154-fold, respectively, without cytotoxicity. These effects likely resulted from the synergic interaction between ME/CI-induced TRP-mediated signaling and CA-activated, TRP-independent signaling. Conclusions: Specific combinations of plant-derived functional components can markedly enhance anti-inflammatory efficacy, supporting dietary strategies that harness multiple phytochemicals for inflammation control and disease prevention. Full article

(This article belongs to the Special Issue Harnessing Natural Bioactives for Sustainable Nutrition and Chronic Disease Control)

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26 pages, 7353 KB

Open AccessArticle

A Multi-Omics Study Reveals the Active Components and Therapeutic Mechanism of Erhuang Quzhi Formula for Non-Alcoholic Fatty Liver Disease

by Teng Ma, Mingzhu Li, Yuan Liu, Yu Chen, Zipeng Guan, Tonghua Liu, Dongmei Qin and Jia Xu

Nutrients 2025, 17(24), 3849; https://doi.org/10.3390/nu17243849 - 10 Dec 2025

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Abstract

Objectives: Erhuang Quzhi Formula (EQF) has been used for the treatment of non-alcoholic fatty liver disease (NAFLD). However, its active components and mechanistic basis remain unclear. This study aims to systematically identify the therapeutic material basis of EQF and to elucidate its potential mechanisms of action against NAFLD through an integrated multi-omics strategy. Methods: An integrated strategy combining UPLC-Q-TOF-MS and network pharmacology was applied to characterize serum components of EQF and construct a compound–target network. Core targets were screened and validated by molecular docking. A NAFLD model was established in C57BL/6 mice through high-fat diet feeding. To evaluate the therapeutic effects, mice were treated with EQF and assessed by measurements of serum biochemical parameters, liver histopathology, and glucose tolerance. UPLC-Q-TOF-based lipidomic and metabolomic analyses of liver tissue were conducted to clarify EQF’s regulatory effects on global lipid profiles and endogenous metabolites. Key genes and proteins involved in relevant signaling pathways were verified by RT-qPCR and Western blot. Results: A total of thirty-one prototype compounds were identified in the EQF-containing serum. Network pharmacology analysis predicted that EQF may alleviate NAFLD by acting on core targets such as TNF, JUN, and STAT3. In vivo experiments demonstrated that EQF administration significantly improved liver function, attenuated dyslipidemia, and reduced inflammation in model mice. Furthermore, metabolomic and lipidomic analyses indicated that EQF effectively reversed abnormal glycerophospholipid and sphingolipid levels and restored their metabolic homeostasis. Conclusions: EQF exerts therapeutic effects in a NAFLD mouse model through multi-component, multi-target, and multi-pathway mechanisms, primarily associated with the regulation of lipid metabolism, improvement of liver function, and suppression of inflammatory responses. This study provides mechanistic insights and a pharmacodynamic basis for the future clinical investigation of EQF. Full article

(This article belongs to the Special Issue Harnessing Natural Bioactives for Sustainable Nutrition and Chronic Disease Control)

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