4.6 Article

Juglans mandshurica leaf extract protects skin fibroblasts from damage by regulating the oxidative defense system

期刊

出版社

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2012.04.013

关键词

Juglans mandshurica MAX.; Anti-oxidative; NF-E2-related factor2; MMP-1; Anti-aging

资金

  1. Ministry of Health & Welfare, Republic of Korea [A103017]
  2. Korea Health Promotion Institute [A103017] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
  3. National Research Foundation of Korea [과06A2601] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

向作者/读者索取更多资源

Skin is mainly damaged by genetic and environmental factors such as ultraviolet light, xenobiotics, hormonal changes, heat, and smoking. ROS production is commonly involved in the pathogenesis of skin damage induced by these factors, causing skin aging, including wrinkling, by activating the metalloproteinases (MMP-1) that break down type I collagen (COL1A1). The walnut tree Juglans mandshurica MAX. (JM) is found in China, Siberia and Korea. JM has been reported to have,various pharmacological activities, such as anti-tumor, anti-oxidative, and anti-bacterial effects. In the present study, we investigated the protective effect of JM leaf extract (JME) against oxidative stress in HS68 human skin fibroblasts. JME significantly and dose-dependently protected HS68 cells against H2O2-induced damage, as assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and lactate dehydrogenase assay. Other assays demonstrated that JME protected HS68 cells by regulating ROS production and increasing levels of glutathione, heme oxygenase-1, and activated NF-E2-related factor 2. JME additionally prevented the elevation of MMP-1 and reduction of COL1A1 induced by H2O2. It also inhibited H2O2-induced phosphorylation of ERK, p38, and JNK. These results indicate that JME protects human skin fibroblasts from H2O2-induced damage by regulating the oxidative defense system. (C) 2012 Elsevier Inc. All rights reserved.

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