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

IF 3.1 4区 生物学 Q3 BIOTECHNOLOGY & APPLIED MICROBIOLOGY
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
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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.

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白菊(牧野)林,北野。花提取物通过调节MAPK信号通路改善氧化应激诱导的HaCaT角质形成细胞损伤。
氧化应激通过促进炎症、细胞凋亡和细胞功能障碍,在皮肤老化和各种皮肤病中起着关键作用。在活性氧(ROS)中,过氧化氢(H2O2)很容易穿透细胞膜,引发氧化损伤。本研究探讨了白菊(dendr菊)的保护作用。花提取物(DBE)抗h2o2诱导的HaCaT角化细胞氧化应激,并探讨其分子机制。DBE (30-80 μg/ml)通过降低cleaved caspase-3的激活和Bax/Bcl-2比值,从而抑制细胞凋亡,显著减弱h2o2诱导的细胞毒性。此外,DBE选择性地抑制JNK和ERK的磷酸化,而对p38 MAPK的激活没有影响。炎症反应也被调节,因为DBE抑制NF-κB p65磷酸化并下调COX-2的表达,COX-2是氧化应激诱导炎症的关键介质。这些发现表明,DBE通过促进细胞存活、抑制细胞凋亡和调节氧化应激和炎症相关的关键信号通路,保护HaCaT角质形成细胞免受氧化应激诱导的细胞损伤。本研究为DBE在预防氧化应激相关皮肤疾病的潜在治疗和美容应用提供了基础见解。
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来源期刊
Journal of microbiology and biotechnology
Journal of microbiology and biotechnology BIOTECHNOLOGY & APPLIED MICROBIOLOGY-MICROBIOLOGY
CiteScore
5.50
自引率
3.60%
发文量
151
审稿时长
2 months
期刊介绍: The Journal of Microbiology and Biotechnology (JMB) is a monthly international journal devoted to the advancement and dissemination of scientific knowledge pertaining to microbiology, biotechnology, and related academic disciplines. It covers various scientific and technological aspects of Molecular and Cellular Microbiology, Environmental Microbiology and Biotechnology, Food Biotechnology, and Biotechnology and Bioengineering (subcategories are listed below). Launched in March 1991, the JMB is published by the Korean Society for Microbiology and Biotechnology (KMB) and distributed worldwide.
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