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
{"title":"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。","authors":"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","doi":"10.4014/jmb.2505.05005","DOIUrl":null,"url":null,"abstract":"<p><p>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 (H<sub>2</sub>O<sub>2</sub>) readily penetrates cell membranes, triggering oxidative damage. This study investigated the protective effects of the <i>Dendranthema boreale</i> (Makino) Ling ex Kitam. flower extract (DBE) against H<sub>2</sub>O<sub>2</sub>-induced oxidative stress in HaCaT keratinocytes and explored the underlying molecular mechanisms. DBE (30-80 μg/ml) significantly attenuated H<sub>2</sub>O<sub>2</sub>-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.</p>","PeriodicalId":16481,"journal":{"name":"Journal of microbiology and biotechnology","volume":"35 ","pages":"e2505005"},"PeriodicalIF":3.1000,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12331467/pdf/","citationCount":"0","resultStr":"{\"title\":\"<i>Dendranthema boreale</i> (Makino) Ling ex Kitam. 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DBE (30-80 μg/ml) significantly attenuated H<sub>2</sub>O<sub>2</sub>-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. 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Dendranthema boreale (Makino) Ling ex Kitam. Flower Extract Ameliorates Oxidative Stress-Induced Cellular Damage in HaCaT Keratinocytes by Regulating MAPK Signaling.
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.
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.