Adenophora remotiflora protects human skin keratinocytes against UVB-induced photo-damage by regulating antioxidative activity and MMP-1 expression.
10.4162/nrp.2016.10.4.371
- Author:
Hye Kyung KIM
1
Author Information
1. Department of Food & Biotechnology, Hanseo University, 46, Hanseo 1-ro, Haemi-Myun, Seosan, Chungnam 31962, Korea. hkkim111@dreamwiz.com
- Publication Type:Original Article
- Keywords:
Adenophora remotiflora;
UVB-irradiation;
HaCaT cell;
antioxidative effect;
MMP-1
- MeSH:
Campanulaceae*;
Cell-Free System;
China;
Collagen;
Collagen Type I;
Humans*;
In Vitro Techniques;
Inhibitory Concentration 50;
Japan;
Keratinocytes*;
Korea;
Metalloproteases;
Nitric Oxide;
Pancreatic Elastase;
Plants;
Reactive Oxygen Species;
RNA, Messenger;
Skin*;
Superoxides
- From:Nutrition Research and Practice
2016;10(4):371-376
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND/OBJECTIVES: Chronic ultraviolet (UV) exposure-induced reactive oxygen species (ROS) are commonly involved in the pathogenesis of skin damage by activating the metalloproteinases (MMP) that break down type I collagen. Adenophora remotiflora (AR) is a perennial wild plant that inhabits Korea, China, and Japan. The present study investigated the protective effects of AR against UVB-induced photo-damage in keratinocytes. MATERIALS/METHODS: An in vitro cell-free system was used to examine the scavenging activity of 2,2-diphenyl-1-picrylhydrazyl (DPPH) free radical and nitric oxide (NO). The effect of AR on ROS formation, antioxidant enzymes, elastase, MMP-1 level, and mRNA expression of MMP-1 were determined in UVB-irradiated human keratinocyte HaCaT cells. RESULTS: AR demonstrated strong DPPH free radical and NO scavenging activity in a cell-free system exhibiting IC50 values of 1.88 mg/mL and 6.77 mg/mL, respectively. AR pretreatment dose-dependently attenuated the production of UVB-induced intracellular ROS, and antioxidant enzymes (catalase and superoxide dismutase) were enhanced in HaCaT cells. Furthermore, pretreatment of AR prevented UVB-induced elastase and collagen degradation by inhibiting the MMP-1 protein level and mRNA expression. Accordingly, AR treatment elevated collagen content in UVB-irradiated HaCaT cells. CONCLUSION: The present study provides the first evidence of AR inhibiting UVB-induced ROS production and induction of MMP-1 as a result of augmentation of antioxidative activity in HaCaT human keratinocytes. These results suggest that AR might act as an effective inhibitor of UVB-modulated signaling pathways and might serve as a photo-protective agent.
