Methanol Extract of Bitter Melon Alleviates UVB-Induced MMPs Expression via MAP Kinase and AP-1 Signaling in Human Dermal Fibroblasts in vitro

被引:24
作者
Lee, Hyun Ji [1 ]
Hwang, Eunson [1 ]
Park, Bom [2 ]
Zhang, Mengyang [1 ]
Sun, Zheng-wang [1 ]
Lee, Do-Gyeong [2 ]
Park, Sang-Yong [1 ]
Yi, Tae Hoo [1 ,2 ]
机构
[1] Kyung Hee Univ, Dept Oriental Med Mat & Proc, Coll Life Sci, Global Campus,1732 Deokyoungdaero, Yongin 446701, Gyeonggi Do, South Korea
[2] Kyung Hee Univ, Coll Life Sci, Grad Sch Biotechnol, Yongin, South Korea
关键词
Bitter melon; photoaging; MMPs; Type I procollagen; MAPK; AP-1; MOMORDICA-CHARANTIA-L; SKIN; PROMOTER; GOURD;
D O I
10.1002/ptr.5656
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
Ultraviolet (UV) irradiation leads to photo-damage of the skin, which in turn induces expression of matrix metalloproteinases (MMPs) and reduces type I procollagen. Bitter melon (Momordica charantia L.) has been widely used as a traditional medicine. In this study, we tested the photo-protective effects of methanol extracts of bitter melon pulp (BM) and the mechanism of these effects in normal human dermal fibroblasts (NHDFs). The effects of BM were investigated by measuring the levels of MMP-1, -3 and -9, and type I procollagen following UVB irradiation. We found that BM alleviates UVB-induced MMP-1, -3 and -9 expression at 100 mu g/mL (down to 52.0%, 73.5%, and 55.6%, respectively). However, cells treated with 100 mu g/mL BM had weakly stimulated type I procollagen expression (up to 130.0%). Moreover, treatment with BM significantly reduced UVB-induced extracellular signal-regulated kinase (ERK), Jun N-terminal kinase (JNK), and p38 phosphorylation, which resulted in decreasing UVB-induced phosphorylation of c-Fos and c-Jun. Therefore, our results suggest that BM is a potential agent for regulating skin photoaging. Copyright (C) 2016 John Wiley & Sons, Ltd.
引用
收藏
页码:1519 / 1526
页数:8
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