Galangin suppresses H₂O₂‐induced aging in human dermal fibroblasts

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 H O . In this study, we established a hydrogen peroxide-induced inflammation and aging model using human HS68 dermal fibroblasts. Stimulation of fibroblasts with H O 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 H O -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.

Extracts of Jasminum sambac flowers fermented by Lactobacillus rhamnosus inhibit H2O2‐ and UVB‐induced aging in human dermal fibroblasts

“…Based on the results of ROS inhibition by F‐FEJS, we next tested whether F‐FEJS would protect fibroblast cells from UVB‐ or H 2 O 2 ‐induced aging. HS68 fibroblast cells were incubated with H 2 O 2 (200 μM) or UVB (40 mJ/cm 2 ) for 24 hours to induce premature senescence 26,27,30 . The levels of aging markers, such as p16, p21, and p53, were significantly upregulated in the H 2 O 2− or UVB‐exposed cells.…”

“…This finding is similar to our previous study. In either high glucose‐induced cardiac cell death or H 2 O 2 ‐induced dermal fibroblast cell damage models, this stress eventually leads to ROS formation and Nrf2 activation 26,43,44 . Interestingly, treatment with F‐FEJS further enhanced antioxidant responses to protect dermal cells from UVB‐ or H 2 O 2 ‐induced damage (Figure 6).…”

“…After UVB exposure, the cells were incubated with different concentrations of F‐FEJS for 24 hours. The cells were exposed to 40 mJ/cm 2 UVB or 200 μM H 2 O 2 because we previously demonstrated that these doses could induce HS68 dermal cell senescence but not apoptosis 26,27 …”

“…HS68 fibroblast cells were incubated with H 2 O 2 (200 μM) or UVB (40 mJ/cm 2 ) for 24 hours to induce premature senescence. 26,27,30 The levels of aging markers, such as p16, p21, and p53, were significantly upregulated in the H 2 O 2− or UVB-exposed cells. However, treatment with F-FEJS (0.1%, 0.5%, and 2.5%) led to a dose-dependent reduction in these aging-related markers ( Figure 3A).…”

“…The cells were exposed to 40 mJ/cm 2 UVB or 200 μM H 2 O 2 because we previously demonstrated that these doses could induce HS68 dermal cell senescence but not apoptosis. 26,27…”