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Protctive effects of Angelicin on UVB-induced HDF cells damage and its mechanism

免疫印迹 雌激素受体 敌手 化学 分子生物学 细胞生长 雌激素 受体 内科学 生物 医学 生物化学 基因 癌症 乳腺癌
作者
Juncen Liu,Haiyang Liu,Guoliang Liu,Yueying Wang,Hainan Gao,Fang Geng
出处
期刊:Traditional Chinese Medicine [Hans Publishers]
卷期号:40 (4): 339-344
标识
DOI:10.3760/cma.j.issn.1673-4246.2018.04.012
摘要

Objective To study the effect of Angelicin on proliferation activity and anti-aging related protein expression of human HDF cells and its mechanism. Methods According to the random number table method, the cells were divided into blank group, model group, estradiol group, Angelicin group, estrogen receptor antagonist+estradiol group, estrogen receptor antagonist+Angelicin group, and P38 pathway blocker group. Different groups were given the according drugs respectively for 24 h. Except the blank group, all the groups of cells were given UVB irradiation with a dose of 150 mJ/cm2. The MTT assay was used to detect cell proliferation rate. The Western blot was used to detect the expression levels of COLⅠ, MMP-1, ERβ, P38 and p-P38 in cells, and the MMP-1 mRNA expression was detected by real-time fluorescent quantitative PCR. Results Compared with the model group, the proliferation rate of HDF cells significantly increased in Angelicin (10, 1, 0.1 and 0.01 μmol/L groups) (P<0.01); The protein expression of COLⅠ (0.326 ± 0.006 vs. 0.176 ± 0.007), ERβ (0.281 ± 0.011 vs. 0.143 ± 0.006) significantly increased (P<0.01), and the expression of MMP-1 (0.256 ± 0.006 vs. 0.395 ± 0.006) and p-P38 (0.224 ± 0.003 vs. 0.318 ± 0.005) significantly decreased (P<0.01) in Angelicin 10 μmol/L group. Compared with 10 μmol/L Angelicin group, the protein expression of estrogen receptor antagonist+Angelicin group ERβ (0.120 ± 0.007 vs. 0.281 ± 0.011) significantly decreased and MMP-1mRNA (1.377 ± 0.012 vs. 1.024 ± 0.010) significantly increased (P<0.01). Conclusions The Angelicin may degrade MMP-1 through the ER-P38 MAPK signaling pathway,and then promote collagen synthesis, to achieve the purpose of prevention and treatment of photoaging. Key words: Angelicin; Estrogen receptor beta; p38 mitogen-activated protein kinases; Collagen; Matrix metalloproteinases; Skin aging

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