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Environ Toxicol. 2017 Dec;32(12):2419-2427. doi: 10.1002/tox.22455. Epub 2017 Aug 18.

Galangin suppresses H2 O2 -induced aging in human dermal fibroblasts.

Author information

1
Department of Dermatology, Taipei City Hospital, Renai Branch, Taipei, Taiwan.
2
Center for General Education, Mackay Junior College of Medicine, Nursing, and Management, Taipei, Taiwan.
3
Department of Biological Science and Technology, College of Biopharmaceutical and Food Sciences, China Medical University, Taichung, Taiwan, ROC.
4
Department of Biology, Georgia State University, Atlanta, Georgia.
5
Division of Breast Surgery, Department of Surgery, China Medical University Hospital, Taichung, Taiwan.
6
Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan.
7
Graduate Institute of Chinese Medical Science, School of Chinese Medicine, China Medical University, Taichung, Taiwan.
8
Department of Health and Nutrition Biotechnology, Asia University, Taichung, Taiwan.

Abstract

Human skin aging is a progressive process that includes intrinsic aging and extrinsic photodamage, both of which can cause an accumulation of reactive oxygen species (ROS), resulting in dermal fibrosis dysfunction and wrinkle formation. Galangin is a flavonoid that exhibits anti-inflammatory and antioxidative potential. Previous studies have reported that galangin has antioxidative activity against ROS-mediated stress. The aim of the present study is to determine the antiaging effects of galangin on dermal fibroblasts exposed to H2 O2 . In this study, we established a hydrogen peroxide-induced inflammation and aging model using human HS68 dermal fibroblasts. Stimulation of fibroblasts with H2 O2 is associated with skin aging and increased expression of inflammation-related proteins, along with downregulation of collagen I/III formation and expression of antioxidative proteins. Galangin effectively reduced NF-κB activation, the expression of inflammation-related proteins and cell aging. Galangin also reversed H2 O2 -activated cell senescence in HS68 cells. Our results reveal that galangin protects human dermal fibroblasts by inhibiting NF-κB activation, decreases the expression of inflammatory factors and upregulates IGF1R/Akt-related proteins, indicating that galangin may be a potential candidate for developing natural antiaging products that protect skin from damage caused by ROS.

KEYWORDS:

anti-inflammatory; antiaging; antioxidation; dermal fibroblasts; galangin

PMID:
28834114
DOI:
10.1002/tox.22455
[Indexed for MEDLINE]

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