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Anti-Inflammatory Diet and Chronic Inflammation

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Nutrition and Metabolism".

Deadline for manuscript submissions: 25 January 2026 | Viewed by 1558

Special Issue Editor


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Guest Editor
South Carolina State University, 1890 Research and Extension, Orangeburg, SC, USA
Interests: Moringa oleifera; anti-inflammatory; vascular disease

Special Issue Information

Dear Colleagues,

Chronic inflammation provides a dominant backdrop to the pathogenesis of several diseases and plays a crucial role. These diseases include inflammatory bowel disease, type 2 diabetes, rheumatoid arthritis, some cancers, and cardiovascular diseases. This pathology (chronic inflammation) is triggered by various abnormalities, such as autoimmune responses, obesity, chronic stress, environmental toxins, and infections through repeated activation of the immune system. Unfortunately, today’s therapies for this ailment, which involve biologics, corticosteroids, and nonsteroidal anti-inflammatory drugs (NSAIDs), are associated with significant limitations, including side-effects, cost, and short-term efficacy, and are based on symptomatic relief.

Lately, reports from studies using dietary interventions in mitigating chronic inflammation demonstrate a potential alternative remedy, with limited side-effects, and addresses the root cause of inflammation. In general, foods such as Moringa, leafy greens, turmeric, nuts, fatty fish, berries, and turmeric have phytochemicals and compounds with anti-inflammatory properties. These dietary components act through their myriad phytochemicals and biologics to mitigate chronic inflammation through the blockage of numerous inflammatory pathways, such as the nuclear factor-kappa B (NF-κB) signaling pathway and the proinflammatory cytokine pathways (TNF-a, IL-6). Of note, these compounds and biologics collectively favor a balanced immune response and include flavonoids, polyphenols, omega-3 fatty acids, curcumin, and modulation of the microbiota.

However, to fully realize the full potential of dietary intervention, we need to understand the underlying mechanisms through which dietary ingredients exert their anti-inflammatory effects, as well as undertake more double-blind clinical trials. These two conditions could potentially pave the way for much safer and cost-effective therapies that could be used to either complement existing therapies or act on their own. This Special Issue reviews several basic and clinical studies by leading authors that have studied various foods with anti-inflammatory activities around the globe, their underlying mechanisms, limitations, and their potential applications in clinical settings.

Dr. Chishimba Nathan Mowa
Guest Editor

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Keywords

  • chronic inflammation
  • diet
  • nutrition
  • anti-inflammation
  • phytochemicals
  • moringa
  • pathogenesis
  • mechanism
  • pathways

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Published Papers (2 papers)

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Research

20 pages, 5193 KB  
Article
Natural Small-Molecule Bergapten Ameliorates Amyloid-β Pathology and Neuroinflammation in Alzheimer’s Disease
by Jingyan Zhang and Jing Zhang
Nutrients 2025, 17(20), 3218; https://doi.org/10.3390/nu17203218 - 14 Oct 2025
Viewed by 573
Abstract
Background: The pathogenesis of Alzheimer’s disease (AD) is complex, and effective treatments remain elusive. Growing evidence suggests that dietary factors may play a significant role in preventing or alleviating AD. Bergapten (BG), a natural compound with anti-inflammatory properties, has been studied; however, its [...] Read more.
Background: The pathogenesis of Alzheimer’s disease (AD) is complex, and effective treatments remain elusive. Growing evidence suggests that dietary factors may play a significant role in preventing or alleviating AD. Bergapten (BG), a natural compound with anti-inflammatory properties, has been studied; however, its specific role in neuroinflammation and AD pathogenesis remains unclear. Methods: Through public databases and bioinformatics tools, the possible molecular mechanisms of BG’s effects on AD were analyzed. Six-month-old 5×FAD mice underwent intragastric administration of BG for 30 consecutive days. Learning and memory abilities were assessed using the novel object recognition (NOR) test and the Morris water maze (MWM) test. Immunofluorescence staining, Western blot and q-PCR was conducted to assess the underlying mechanisms. In vitro experiments used Aβ-stimulated BV2 microglial cells for BG intervention. Results: Bioinformatics analysis revealed the MAPK signaling pathway as the top-ranked pathway. Molecular docking studies further demonstrated strong binding interactions between BG and key proteins within the MAPK pathway. In behavioral studies, NOR test and MWM test demonstrated that BG treatment improved learning and memory abilities in 5×FAD mice. Additionally, BG treatment significantly reduced Aβ deposition, pro-inflammatory cytokine levels, and inhibited excessive microglial activation in these mice. Consistent with in vivo findings, BG effectively decreased pro-inflammatory cytokines in Aβ-stimulated BV2 microglial cells. Mechanistic studies revealed that BG attenuates neuroinflammatory responses by inhibiting the MAPK signaling pathway both in vivo and in vitro. Conclusions: Our findings suggest that BG mitigates AD pathological features by suppressing MAPK-mediated neuroinflammation and represents a promising natural small molecule for the prevention and treatment of AD. Full article
(This article belongs to the Special Issue Anti-Inflammatory Diet and Chronic Inflammation)
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15 pages, 1662 KB  
Article
Eicosapentaenoic Acid and Urolithin a Synergistically Mitigate Heat Stroke-Induced NLRP3 Inflammasome Activation in Microglial Cells
by Hyunji Cho, Judy Kim, Yongsoon Park, Young-Cheul Kim and Soonkyu Chung
Nutrients 2025, 17(19), 3063; https://doi.org/10.3390/nu17193063 - 25 Sep 2025
Viewed by 529
Abstract
Background/Objectives: Global warming and concomitant extreme weather events have markedly increased the incidence of heat stroke. Heat stroke (HS) poses a substantial threat to cerebral health by triggering neuroinflammation and accelerating neurodegenerative processes. The activation of the Nod-like receptor protein 3 (NLRP3) [...] Read more.
Background/Objectives: Global warming and concomitant extreme weather events have markedly increased the incidence of heat stroke. Heat stroke (HS) poses a substantial threat to cerebral health by triggering neuroinflammation and accelerating neurodegenerative processes. The activation of the Nod-like receptor protein 3 (NLRP3) inflammasome for interleukin-1β (IL-1β) secretion has been implicated as a critical mechanism underlying HS-related fatalities. However, the potential role of specific dietary factors to counteract heat stroke-induced neurotoxicity remains largely underexplored. We previously reported that eicosapentaenoic acid (EPA) and urolithin A (UroA), a gut metabolite of ellagic acid, effectively suppress NLRP3 inflammasome activation against metabolic or pathogenic insults. This study aimed to assess the impact of eicosapentaenoic acid (EPA), urolithin A (UroA), and their combination on mitigating heatstroke-mediated NLRP3 inflammasome activation in microglial cells. Methods: In vitro heatstroke conditions were replicated by subjecting murine BV2 microglial cells to a high temperature (41 °C) under hypoxic conditions. To achieve nutrient loading, BV2 cells were preincubated with either EPA (50 µM) or UroA (10 µM). NLRP3 inflammasome activation was evaluated by proinflammatory gene expression, caspase-1 cleavage in cells, and IL-1β secretion to the medium. The caspase-1 activation was determined using a luciferase-based inflammasome and protease activity reporter (iGLuc) assay. Results: Exposure to high temperatures under hypoxia successfully mimicked HS conditions and promoted NLRP3 inflammasome activation in BV2 cells. Both EPA and UroA substantially attenuated the heat stroke-induced priming of proinflammatory genes. More importantly, EPA and UroA demonstrated a synergistic effect in mitigating HS-induced active caspase-1 production, leading to a dramatic decrease in IL-1β secretion. This synergistic effect between EPA and UroA was further confirmed by the iGLuc reporter assay. Conclusions: Dietary enrichment with EPA and UroA precursors may constitute an efficacious strategy for mitigating heat stroke-mediated neuroinflammation and neurodegenerative diseases. Full article
(This article belongs to the Special Issue Anti-Inflammatory Diet and Chronic Inflammation)
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