摘要
The attenuation of atopic dermatitis (AD) by Camellia oil was investigated in Raw 264.7 macrophages and HaCaT keratinocytes cell lines in this paper. Results showed that phenolic-abundant Camellia oil (PACO) by the AEE method showed the lowest expression levels of pro-inflammatory cytokines, including TNF-α, IL-6 and IL-1β in LPS-induced Raw 264.7 cells, followed by the cold-pressed Camellia oil (CPCO), then the commercial refined Camellia oil (CRCO). This may be attributed to a higher content of polyphenols in PACO, particularly for typical phenolics such as caffeic acid, quercetin, kaempferol, kaempferol-3-O-[2-O-β-D-galactopyranosyl-6-O-α-L-rhamnopyranosyl]-β-D-glucopyranoside (KGRG) and kaempferol-3-O-[2-O-β-D-xylopyranosyl-6-O-α-L-rhamnopyranosyl]-β-D-glucopyranoside (KXR), which are associated with lower NO levels in model cells and higher antioxidant capacities in DPPH, ABTS, and FRAP experiments. In HaCaT keratinocytes, exposure to TNF-α/IFN-γ resulted in an 8-fold and 10-fold increase in CCL-17 and IL-33, compared with control , indicating skin inflammation occurred. Camellia oil treatment improved this inflammation, embodied by a significant restoration of skin inflammatory mediators, and this improvement is dose-dependent. High-dose PACO exhibited the best anti-skin inflammatory effects. The mRNA expression levels of MMP1 , MMP9 , MMP25 , VEGFC and TNFRSF6B were also significantly down-regulated after PACO treatment, indicating its potential for skin barrier protection. Moreover, 800 μg/mL PACO significantly alleviated the cell apoptosis rate and regulated the apoptosis-related biomarkers at gene expression and protein expression levels ( Bax , Bcl-2 and Caspase-3 ). Analysis results on the JC-1 ΔΨm and mitochondrial ROS indicated that mitochondrial damage was reversed after the Camellia oil treatment, which accounted for its alleviation effects on apoptosis related to inflammation. Overall, Camellia oil, rich in phenolics, exhibited great therapeutic potential for AD treatment.
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