# Avenanthramide C From Oats Possibly Exerts Anti‐Inflammatory Effects in Human Umbilical Vein Endothelial Cells

**Authors:** Hiroyuki Sasaki, Hirofumi Masutomi, Hajime Nagasawa, Yuma Matsumoto, Teruyuki Okuma, Tomoyuki Otsuka, Katsuyuki Ishihara, Yusuke Suzuki, Seiji Ueda

PMC · DOI: 10.1111/1750-3841.70841 · Journal of Food Science · 2026-01-09

## TL;DR

A compound in oats may reduce inflammation in blood vessels of people with kidney disease.

## Contribution

Avenanthramide C from oats is shown to suppress inflammation caused by a uremic toxin in endothelial cells.

## Key findings

- Avenanthramide C suppresses IS-induced IL-6 secretion in HUVECs.
- Avenanthramide C interacts with AhR and inhibits AhR target gene expression.
- Anti-inflammatory effects of avenanthramide C are independent of several signaling pathways.

## Abstract

Chronic kidney disease (CKD) is associated with inflammation and cardiovascular complications and is partly exacerbated by the uremic toxin indoxyl sulfate (IS). IS is known to activate the aryl hydrocarbon receptor (AhR) to promote vascular inflammation. On the other hand, avenanthramide C (Ave), an oat‐derived polyphenol, has antioxidative and anti‐inflammatory properties. Therefore, we investigated whether Ave can suppress IS‐induced inflammatory responses.

Analysis of serum from hemodialysis patients revealed a significant correlation between IS and interleukin‐6 (IL‐6) levels. In human umbilical vein endothelial cells (HUVECs), IS (≥50 µg/mL) increased IL‐6 secretion, while Ave (≥10 µM) suppressed this effect. Docking simulations and in vitro experiments suggested that Ave may interact with AhR and suppress IS‐induced expression of AhR target genes, including that of cytochrome P450 family 1 subfamily A member 1. High‐performance liquid chromatography verified the uptake of Ave by human umbilical vein endothelial cells. Additionally, the anti‐inflammatory effects of Ave were independent of the adrenergic α1 receptor, adenosine monophosphate‐activated protein kinase pathways, and protein kinase B pathways.

Ave suppresses IS‐induced inflammation, thereby reducing IL‐6 secretion in HUVECs. These findings suggest the potential of Ave as a dietary intervention for mitigating vascular inflammation in patients with CKD.

## Linked entities

- **Genes:** AHR (aryl hydrocarbon receptor) [NCBI Gene 196], CYP1A1 (cytochrome P450 family 1 subfamily A member 1) [NCBI Gene 1543]
- **Chemicals:** avenanthramide C (PubChem CID 11723200), indoxyl sulfate (PubChem CID 10258)
- **Diseases:** chronic kidney disease (MONDO:0005300)
- **Species:** Homo sapiens (taxon 9606)

## Full-text entities

- **Genes:** CYP1A1 (cytochrome P450 family 1 subfamily A member 1) [NCBI Gene 1543] {aka AHH, CP11, CYP1, CYPIA1, P1-450, P450-C}, PTK2B (protein tyrosine kinase 2 beta) [NCBI Gene 2185] {aka CADTK, CAKB, FADK2, FAK2, PKB, PTK}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, AHR (aryl hydrocarbon receptor) [NCBI Gene 196] {aka FVH3, RP85, bHLHe76}
- **Diseases:** uremic (MESH:D006463), cardiovascular complications (MESH:D002318), Inflammatory (MESH:D007249), CKD (MESH:D051436)
- **Chemicals:** polyphenol (MESH:D059808), Ave (MESH:C514463), IS (MESH:D007200)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12785505/full.md

## References

50 references — full list in the complete paper: https://tomesphere.com/paper/PMC12785505/full.md

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Source: https://tomesphere.com/paper/PMC12785505