Protective Effects of Standardized Siegesbeckia glabrescens Extract and Its Active Compound Kirenol against UVB-Induced Photoaging through Inhibition of MAPK/NF-κB Pathways원문보기
Anti-photoaging effects of standardized Siegesbeckia glabrescens extract (SGE) and its major active compound kirenol were investigated using Hs68 human dermal fibroblasts and hairless mice, respectively. UVB-irradiated hairless mice that received oral SGE (600 mg/kg/day) showed reduced wrinkle forma...
Anti-photoaging effects of standardized Siegesbeckia glabrescens extract (SGE) and its major active compound kirenol were investigated using Hs68 human dermal fibroblasts and hairless mice, respectively. UVB-irradiated hairless mice that received oral SGE (600 mg/kg/day) showed reduced wrinkle formation and skinfold thickness compared with the UVB-irradiated control. Furthermore, SGE treatment increased the mRNA levels of collagen synthesis genes (COL1A1, COL3A1, COL4A1, and COL7A1) and activated antioxidant enzyme (catalase), while suppressing matrix metalloproteinase (MMP-2, -3, -9, and -13) expression. In Hs68 fibroblasts, kirenol also significantly suppressed MMP expression while increasing the expression of COL1A1, COL3A1, and COL7A1. Collectively, our data demonstrate that both SGE and kirenol attenuated UVB-induced photoaging in hairless mice and fibroblasts through inhibition of the mitogen-activated protein kinases and nuclear factor kappa B pathways, suggesting that SGE has potential to serve as a natural anti-photoaging nutraceutical.
Anti-photoaging effects of standardized Siegesbeckia glabrescens extract (SGE) and its major active compound kirenol were investigated using Hs68 human dermal fibroblasts and hairless mice, respectively. UVB-irradiated hairless mice that received oral SGE (600 mg/kg/day) showed reduced wrinkle formation and skinfold thickness compared with the UVB-irradiated control. Furthermore, SGE treatment increased the mRNA levels of collagen synthesis genes (COL1A1, COL3A1, COL4A1, and COL7A1) and activated antioxidant enzyme (catalase), while suppressing matrix metalloproteinase (MMP-2, -3, -9, and -13) expression. In Hs68 fibroblasts, kirenol also significantly suppressed MMP expression while increasing the expression of COL1A1, COL3A1, and COL7A1. Collectively, our data demonstrate that both SGE and kirenol attenuated UVB-induced photoaging in hairless mice and fibroblasts through inhibition of the mitogen-activated protein kinases and nuclear factor kappa B pathways, suggesting that SGE has potential to serve as a natural anti-photoaging nutraceutical.
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문제 정의
Clinical symptoms of UV-irradiated skin photoaging include dryness, roughness, hyperpigmentation, coarse elastosis, and laxity [9]. This study investigated whether SGE protects UVB-induced photoaging by assaying histological and clinical changes in hairless mice. UVB irradiation increased the formation of wrinkles in the dorsal skin of control mice; however, SGE treatment significantly reduced it, as seen in the UVB + SGE 600-treated mice (Fig.
제안 방법
Hematoxylin and eosin (H&E) staining for measuring skin thickness, Masson’s trichrome (M&T) staining for measuring collagen fiber, and Verhoeff-van Gieson’s staining for measuring elasticity were performed on skin tissue sections.
This study was the first to demonstrate that SGE, and its active compound kirenol, prevents UVB-induced photoaging by regulating MMP expression and collagen degradation, in addition to suppressing oxidative stress and the associated intracellular MAPK/NF-κB pathways.
대상 데이터
Fifteen 5-week-old female albino hairless mice (SKH-1; Daehan Biolink Ltd., Korea) were maintained in a humidity-, temperature-, and light-controlled specific pathogen-free room (55 ± 10% humidity, 23 ± 2℃, and 12 h light/dark cycle) at Yonsei Laboratory Animal Research Center (Korea).
Hematoxylin and eosin (H&E) staining for measuring skin thickness, Masson’s trichrome (M&T) staining for measuring collagen fiber, and Verhoeff-van Gieson’s staining for measuring elasticity were performed on skin tissue sections. The stained skin area was examined using the Eclipse TE2000U Inverted Microscope with twin CCD cameras (Nikon, Japan).
데이터처리
The differences of groups were evaluated by unpaired Student’s t-test for in vivo data.
이론/모형
Cell viability was assessed by MTT assay. Hs68 human skin fibroblasts were treated to various doses of kirenol (0 to 60 μM).
Homogenized skin tissues and Hs68 cells were lysed with RIPA buffer (ELPIS-Biotech) containing protease inhibitor cocktails. Total protein concentrations were quantified by the Bradford assay. Equal 30 μg amounts of protein were size-fractionated by 10% sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and transferred to membranes.
성능/효과
This study showed that the SGE treatment group demonstrated lower UVB-induced phosphorylation of MAPK components, including ERK, JNK, and p38, than the control group (Fig. 4B). Furthermore, the SGE treatment decreased the protein levels of AP-1 complex components, such as c-Jun and c-Fos, compared with the UVB-irradiated control (Fig.
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