Camellia sinensis Seed Flavonoids Attenuate UVB-Induced Inflammation and UVA-Induced Photodamage via MAPK/NF-κB and AP-1 Pathways

TL;DR

This study shows that Camellia sinensis seed flavonoids can reduce UV-induced skin damage and inflammation by targeting specific cellular pathways.

Contribution

The study reveals the novel anti-inflammatory and anti-photoaging mechanisms of Camellia sinensis seed flavonoids via MAPK/NF-κB and AP-1 pathways.

Findings

CSF reduced ROS and inflammatory factors in keratinocytes via p38/JNK and NF-κB inhibition.

CSF upregulated skin barrier proteins and counteracted UVA damage in fibroblasts via AP-1 and TGF-β/Smad pathways.

CSF demonstrated coordinated anti-inflammatory, barrier-repair, and anti-photoaging effects.

Abstract

This study evaluated the anti-inflammation and anti-photoaging effects of Camellia sinensis seed flavonoids (CSF) against UVB and UVA irradiation and elucidated the underlying mechanisms. Using UVB-irradiated human keratinocytes and UVA-irradiated human dermal fibroblasts, we found that CSF significantly reduced intracellular ROS and suppressed the secretion of inflammatory factors (PGE-2, TNF-α, IL-6, IL-8) by inhibiting the p38/JNK and NF-κB pathways, along with iNOS and COX-2 expression. In keratinocytes, CSF also downregulated Caspase-3 and upregulated barrier proteins filaggrin and Claudin-1. In fibroblasts, CSF counteracted UVA damage by upregulating collagen IV and XVII at the dermo-epidermal junction and enhancing the production of collagen I, III, and hyaluronic acid in the dermis, mediated via AP-1 inhibition and TGF-β/Smad pathway modulation. These results demonstrate that CSF coordinated anti-inflammatory, barrier-repair, and anti-photoaging actions, highlighting its potential as a promising skincare ingredient.

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