# Chrysotoxine Attenuates Key Atherogenic Processes via Antioxidant, Anti-Inflammatory, and COX-Dependent Antiplatelet Mechanisms

**Authors:** Fozia Rustamani, Hla Nu Swe, Su Wutyi Thant, Jeeradej Moonrut, Boonchoo Sritularak, Ponlapat Rojnuckarin, Nonthaneth Nalinratana, Rataya Luechapudiporn

PMC · DOI: 10.3390/biom16030379 · Biomolecules · 2026-03-03

## TL;DR

Chrysotoxine, a compound from a plant, shows potential in fighting atherosclerosis by reducing harmful processes like inflammation and platelet activation.

## Contribution

The study reveals chrysotoxine's multi-target anti-atherogenic mechanisms, including COX-dependent antiplatelet activity.

## Key findings

- Chrysotoxine significantly reduced hemin-induced LDL oxidation and apolipoprotein modification.
- It inhibited lipopolysaccharide-induced monocyte adhesion in an endothelial–monocyte co-culture model.
- Chrysotoxine inhibited platelet aggregation and showed COX-1 and COX-2 inhibitory activity in low micromolar ranges.

## Abstract

Atherosclerosis is a complex vascular disorder driven by oxidative stress, inflammation, and platelet activation. Agents capable of targeting multiple atherogenic pathways may provide improved therapeutic benefits. In this study, we evaluated the anti-atherogenic effects of chrysotoxine, a bibenzyl compound isolated from Dendrobium pulchellum, using in vitro models relevant to atherogenesis. Chrysotoxine significantly suppressed hemin-induced LDL oxidation by reducing lipid peroxidation and apolipoprotein modification. In an endothelial–monocyte co-culture model, chrysotoxine markedly attenuated lipopolysaccharide-induced monocyte adhesion, indicating inhibition of endothelial inflammatory activation. Chrysotoxine also inhibited platelet aggregation induced by arachidonic acid, ADP, and collagen in a concentration-dependent manner, with the strongest effects observed against arachidonic acid–mediated responses, suggesting modulation of the thromboxane pathway. Molecular docking analyses and cyclooxygenase activity assays further indicated that chrysotoxine may interact with both COX-1 and COX-2, exhibiting inhibitory activity in the low micromolar range. Collectively, these findings demonstrate that chrysotoxine modulates multiple key processes involved in atherogenesis, including oxidative LDL modification, vascular inflammation, and platelet activation. Although further in vivo studies are required, chrysotoxine represents a promising plant-derived candidate for the development of multi-target strategies against atherosclerotic disease.

## Linked entities

- **Chemicals:** chrysotoxine (PubChem CID 5315860), hemin (PubChem CID 26945), arachidonic acid (PubChem CID 444899), ADP (PubChem CID 6022)
- **Diseases:** atherosclerosis (MONDO:0005311)
- **Species:** Dendrobium pulchellum (taxon 671528)

## Full-text entities

- **Genes:** COX1 (cytochrome c oxidase subunit I) [NCBI Gene 4512] {aka COI, MTCO1}, COX2 (cytochrome c oxidase subunit II) [NCBI Gene 4513] {aka COII, MTCO2}, COX8A (cytochrome c oxidase subunit 8A) [NCBI Gene 1351] {aka COX, COX8, COX8-2, COX8L, MC4DN15, VIII}
- **Diseases:** Atherogenic (MESH:D050197), platelet aggregation (MESH:D001791), Inflammatory (MESH:D007249), vascular disorder (MESH:D002561)
- **Chemicals:** lipid (MESH:D008055), ADP (MESH:D000244), bibenzyl compound (-), hemin (MESH:D006427), lipopolysaccharide (MESH:D008070), Chrysotoxine (MESH:C555497), thromboxane (MESH:D013931), arachidonic acid (MESH:D016718)
- **Species:** Dendrobium pulchellum (species) [taxon 671528]

## Full text

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## Figures

8 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13024289/full.md

## References

74 references — full list in the complete paper: https://tomesphere.com/paper/PMC13024289/full.md

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Source: https://tomesphere.com/paper/PMC13024289