Phytocosmetic potential of Blumea balsamifera oil in mitigating UV-induced photoaging: Evidence from cellular and mouse models
文献类型: 外文期刊
作者: Wang, Kai 1 ; Hu, Xuan 1 ; Xie, Xiao-Li 1 ; Huang, Mei 1 ; Wang, Dan 1 ; Yu, Fu-Lai 1 ;
作者机构: 1.Chinese Acad Trop Agr Sci, Trop Crops Genet Resources Inst, Key Lab Biol & Cultivat Herb Med Haikou, Minist Agr & Rural Affairs, Haikou 571101, Hainan, Peoples R China
2.Hainan Prov Engn Res Ctr Blumea Balsamifera, Haikou 571101, Hainan, Peoples R China
关键词: Cellular senescence; Skin aging; Blumea balsamifera oil; Matrix metalloproteinases; Antioxidation; Anti-inflammation
期刊名称:JOURNAL OF ETHNOPHARMACOLOGY ( 影响因子:5.4; 五年影响因子:5.4 )
ISSN: 0378-8741
年卷期: 2024 年 334 卷
页码:
收录情况: SCI
摘要: Ethnopharmacological relevance: Blumea balsamifera (L.) DC. (BB), the source of Blumea balsamifera oil (BBO), is an aromatic medicinal plant, renowned for its pharmacological properties and its traditional use in Southeast Asian countries such as China, Thailand, Vietnam, Malaysia, and the Philippines for centuries. Traditionally, BB has been used as a raw herbal medicine for treating various skin conditions like eczema, dermatitis, athlete's foot, and wound healing for skin injuries. Aim of the study: This research aimed to explore the inhibitory effects of BBO on skin aging using two models: in vitro analysis with human dermal fibroblasts (HDF) under UVB-induced stress, and in vivo studies on UVAinduced dorsal skin aging in mice. The study sought to uncover the mechanisms behind BBO's anti-aging effects, specifically, its impact on cellular and tissue responses to UV-induced skin aging. Materials and methods: We applied doses of 10-20 mu L/mL of BBO to HDF cells that had been exposed to UVB radiation to simulate skin aging. We measured cell viability, and levels of reactive oxygen species (ROS), SA- n-gal, pro-inflammatory cytokines, and matrix metalloproteinases (MMPs). In addition, we investigated the involvement of mitogen-activated protein kinases (MAPKs) and nuclear factor kappa B (NF-kappa B) signaling pathways in mediating the anti-aging effects of BBO. Histopathological and biochemical analyses were conducted in a mouse model to examine the effects of BBO on UV-induced photoaging. Results: UV exposure accelerated aging, and caused cellular damage and inflammatory responses through ROSmediated pathways. In HDF cells, BBO treatment countered the UVB-induced senescence, and the recovery of cell viability was correlated to notable reductions in SA-n-gal, ROS, pro-inflammatory cytokines, and MMPs. Mechanistically, the anti-aging effect of BBO was associated with the downregulation of the JNK/NF-kappa B signaling pathways. In the in vivo mouse model, BBO exhibited protective capabilities against UV-induced photoaging, which were manifested by the enhanced antioxidant enzyme activities and tissue remodeling. Conclusions: BBO effectively protects fibroblasts from UV-induced photoaging through the JNK/NF-kappa B pathway. Recovery from photoaging involves an increase in dermal fibroblasts, alleviation of inflammation, accelerated synthesis of antioxidant enzymes, and slowed degradation of ECM proteins. Overall, BBO enhances the skin's defensive capabilities against oxidative stress, underscoring its potential as a therapeutic agent for oxidative stress-related skin aging.
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