Dendrobium nobile Lindl. Polysaccharides protect fibroblasts against UVA-induced photoaging via JNK/c-Jun/MMPs pathway

光老化 超氧化物歧化酶 化学 活性氧 谷胱甘肽过氧化物酶 氧化应激 活力测定 丙二醛 过氧化氢酶 抗氧化剂 谷胱甘肽 脂质过氧化 基质金属蛋白酶 药理学 生物化学 细胞凋亡 生物 遗传学
作者
Wei Li,Xingrui Mu,Xingqian Wu,Wenjie He,Ye Liu,Yiqiu Liu,Junyu Deng,Xuqiang Nie
出处
期刊:Journal of Ethnopharmacology [Elsevier BV]
卷期号:298: 115590-115590 被引量:47
标识
DOI:10.1016/j.jep.2022.115590
摘要

ETHNOPHARMACOLOGICAL RELEVANCE: Dendrobium nobile Lindl. is an orchid species that is found throughout Asia, including Thailand, Laos, Vietnam, and China. It has been used to treat tumors, hyperglycemia, hyperlipidemia, and neurological disorders caused by aging in recent decades. AIM OF THE STUDY: To investigate the antagonistic effect of Dendrobium nobile Lindl. Polysaccharides (DNLP) on UVA-induced photoaging of Human foreskin fibroblasts (HFF-1) and explore its possible anti-aging mechanisms. MATERIALS AND METHODS: An in vitro photoaging model of dermal fibroblasts was established with multiple UVA irradiations. Fibroblasts were treated with 0.06 mg/ml, 0.18 mg/ml, 0.54 mg/ml of DNLP one day before photodamage induction. The levels of reactive oxygen species (ROS), Malondialdehyde (MDA), cell viability and longevity, Superoxide Dismutase (SOD), Catalase (CAT), and Glutathione peroxidase (GSH-Px) enzymatic activities were determined. We examined how DNLP ameliorates the effects of photoaging, the JNK/c-Fos/c-Jun pathway, senescence-associated β-galactosidase (SA-β-Gal), and MMP expression levels were measured. RESULTS: UVA irradiation reduced the viability, lifespan, and proliferation of HFF-1 cells, increased ROS and lipid peroxidation and decreased the activities of free radical scavenging enzyme systems SOD, CAT, and GSH-Px. DNLP treatment can reverse UVA damage, reduce SA-β-Gal expression, reduce phosphorylation activation of the JNK/c-Fos/c-Jun pathway and inhibit MMP-1, MMP-2 MMP-3, and MMP-9 protein expression. CONCLUSIONS: DNLP can effectively inhibit UVA damage to HFF-1 and prevent cell senescence. Its mechanism of action may increase antioxidant enzyme activity while inhibiting JNK pathway activation and MMPs expression.
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