# Harnessing Anthocyanins to Mitigate Inflammation, Dysbiosis, and Aging in the Gastrointestinal Tract

**Authors:** Livia Resende Lopes, Adriel Aparecido de Souza, Tanila Wood dos Santos, Raquel de Cássia dos Santos

PMC · DOI: 10.1021/acsptsci.5c00566 · ACS Pharmacology & Translational Science · 2026-01-28

## TL;DR

This review explores how anthocyanins, plant pigments, can reduce gut inflammation, restore microbial balance, and counteract aging effects in the gastrointestinal tract.

## Contribution

The paper systematically reviews how anthocyanins modulate gut microbiota, reduce inflammation, and mitigate aging in the gut, offering a novel dietary therapeutic approach.

## Key findings

- Anthocyanins suppress pro-inflammatory cytokines like interleukin-1β, interleukin-6, TNF-α, and interferon-γ.
- They restore microbial balance, promote short-chain fatty acid synthesis, and preserve mucosal architecture.
- In aging models, anthocyanins reduce oxidative stress, inhibit senescence signaling, and restore anti-inflammatory interleukin-10 levels.

## Abstract

The gut microbiota are a dynamic ecosystem that is crucial
for
immune regulation and maintenance of intestinal barrier integrity.
Dysbiosis within this community contributes to the chronic inflammation
characteristic of inflammatory bowel diseases (IBD), including Crohn’s
disease and ulcerative colitis, for which no definitive cure currently
exists. This comprehensive review examines recent preclinical and
clinical studies on how anthocyanin-polyphenolic pigments, such as
cyanidins and malvidins, modulate gut microbial communities, reduce
intestinal inflammation, and counteract age-related declines in immune
homeostasis. We analyzed the literature on anthocyanin–microbiota
interactions in IBD pathogenesis, focusing on cytokine profiles, barrier
function assays, lipopolysaccharide synthesis, oxidative stress markers,
and short-chain fatty acid production. Additionally, we explored the
relationship among cellular senescence, the senescence-associated
secretory phenotype (SASP), and microbiome shifts during intestinal
aging. Evidence indicates that anthocyanins consistently suppress
key pro-inflammatory cytokines, such as interleukin-1β, interleukin-6,
TNF-α, and interferon-γ, while preserving mucosal architecture
and reducing lipopolysaccharide load and mitochondrial oxidative phosphorylation.
These compounds help to restore microbial balance, promote short-chain
fatty acid synthesis, and enrich bacterial taxa associated with barrier
integrity. In aging models, anthocyanins attenuate oxidative stress,
stabilize redox homeostasis, inhibit senescence signaling and SASP
secretion, and partially restore anti-inflammatory interleukin-10
levels. In conclusion, anthocyanins are promising dietary therapeutics
for IBD management and for mitigating intestinal aging. Future research
should transition from murine models to human clinical trials by integrating
senolytic strategies, targeted microbiome modulation, and pharmacological
dissection of the senescence–microbiome axis to foster disease
prevention and promote healthy aging.

## Linked entities

- **Chemicals:** anthocyanins (PubChem CID 145858)
- **Diseases:** Crohn’s disease (MONDO:0005011), ulcerative colitis (MONDO:0005101)

## Full-text entities

- **Genes:** IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, IL10 (interleukin 10) [NCBI Gene 3586] {aka CSIF, GVHDS, IL-10, IL10A, TGIF}, IFNG (interferon gamma) [NCBI Gene 3458] {aka IFG, IFI, IMD69}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}
- **Diseases:** Dysbiosis (MESH:D064806), Inflammation (MESH:D007249), ulcerative colitis (MESH:D003093), IBD (MESH:D015212), Crohn's disease (MESH:D003424)
- **Chemicals:** Anthocyanins (MESH:D000872), short-chain fatty acid (MESH:D005232), lipopolysaccharide (MESH:D008070), cyanidins (MESH:C017154), malvidins (MESH:C065861)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Homo sapiens (human, species) [taxon 9606]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12910501/full.md

## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12910501/full.md

## References

100 references — full list in the complete paper: https://tomesphere.com/paper/PMC12910501/full.md

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Source: https://tomesphere.com/paper/PMC12910501