# Dendranthema boreale (Makino) Ling ex Kitam. Flower Extract Ameliorates Oxidative Stress-Induced Cellular Damage in HaCaT Keratinocytes by Regulating MAPK Signaling

**Authors:** You Kyeong Lee, Parkyong Song, Seo Young Choi, Mi Song Shin, Ji Sun Hwang, Hong-Joo Son, Yu-Jin Kim, Wanil Kim, Kwang Min Lee

PMC · DOI: 10.4014/jmb.2505.05005 · Journal of Microbiology and Biotechnology · 2025-07-18

## TL;DR

This study shows that Dendranthema boreale flower extract protects skin cells from oxidative stress by reducing cell death and inflammation.

## Contribution

The study reveals the novel protective mechanism of Dendranthema boreale extract against oxidative stress via MAPK signaling modulation.

## Key findings

- DBE reduced H2O2-induced cytotoxicity by inhibiting apoptosis in HaCaT cells.
- DBE suppressed JNK and ERK phosphorylation without affecting p38 MAPK activation.
- DBE inhibited NF-κB p65 phosphorylation and COX-2 expression, reducing inflammation.

## Abstract

Oxidative stress plays a critical role in skin aging and in various dermatological disorders by promoting inflammation, apoptosis, and cellular dysfunction. Among reactive oxygen species (ROS), hydrogen peroxide (H2O2) readily penetrates cell membranes, triggering oxidative damage. This study investigated the protective effects of the Dendranthema boreale (Makino) Ling ex Kitam. flower extract (DBE) against H2O2-induced oxidative stress in HaCaT keratinocytes and explored the underlying molecular mechanisms. DBE (30-80 μg/ml) significantly attenuated H2O2-induced cytotoxicity by reducing cleaved caspase-3 activation and lowering the Bax/Bcl-2 ratio, thereby inhibiting apoptosis. Furthermore, DBE selectively suppressed JNK and ERK phosphorylation while having no effect on p38 MAPK activation. Inflammatory responses were also modulated, as DBE inhibited NF-κB p65 phosphorylation and downregulated COX-2 expression, a key mediator of oxidative stress-induced inflammation. These findings indicate that DBE protects HaCaT keratinocytes from oxidative stress-induced cellular damage by promoting cell survival, suppressing apoptosis, and modulating the key signaling pathways involved in oxidative stress and inflammation. This study provides foundational insights into the potential therapeutic and cosmetic applications of DBE for the prevention of oxidative stress-related skin disorders.

## Linked entities

- **Genes:** BAX (BCL2 associated X, apoptosis regulator) [NCBI Gene 581], BCL2 (BCL2 apoptosis regulator) [NCBI Gene 596], COX2 (cytochrome c oxidase subunit II) [NCBI Gene 4513]
- **Proteins:** Casp3 (caspase 3), MAPK8 (mitogen-activated protein kinase 8), EPHB2 (EPH receptor B2), P38mapk (p38 map kinase)
- **Chemicals:** H2O2 (PubChem CID 784)

## Full-text entities

- **Diseases:** cytotoxicity (MESH:D064420), dermatological (MESH:D000168), Inflammatory (MESH:D007249), skin disorders (MESH:D012871)
- **Chemicals:** DBE (-), H2O2 (MESH:D006861), ROS (MESH:D017382)
- **Species:** Chrysanthemum boreale (species) [taxon 344871]
- **Cell lines:** HaCaT — Homo sapiens (Human), Spontaneously immortalized cell line (CVCL_0038)

## Full text

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## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12331467/full.md

## References

43 references — full list in the complete paper: https://tomesphere.com/paper/PMC12331467/full.md

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Source: https://tomesphere.com/paper/PMC12331467