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黄钟花通过抑制 MMPs、MAP 激酶、COX-2 的表达和促进 I 型前胶原合成来防止 UVB 诱导的光老化。

Ixora parviflora Protects against UVB-Induced Photoaging by Inhibiting the Expression of MMPs, MAP Kinases, and COX-2 and by Promoting Type I Procollagen Synthesis.

机构信息

Department of Cosmecutics, China Medical University, Taichung 404, Taiwan.

出版信息

Evid Based Complement Alternat Med. 2012;2012:417346. doi: 10.1155/2012/417346. Epub 2011 Dec 1.

DOI:10.1155/2012/417346
PMID:22203872
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3235733/
Abstract

Ixora parviflora with high polyphenol content exhibited antioxidant activity and reducing UVB-induced intracellular reactive oxygen species production. In this study, results of the photoaging screening experiments revealed that IPE at 1000 μg/mL reduced the activity of bacterial collagenase by 92.7 ± 4.2% and reduced the activity of elastase by 32.6 ± 1.4%. Therefore, we investigated the mechanisms by which IPE exerts its anti-photoaging activity. IPE at 1 μg/mL led to an increase in type I procollagen expression and increased total collagen synthesis in fibroblasts at 5 μg/mL. We found that IPE inhibited MMP-1, MMP-3, and MMP-9 expression at doses of 1, 5, and 10 μg/mL, respectively, in fibroblasts exposed to UV irradiation (40 mJ/cm(2)). Gelatin zymography assay showed that IPE at 50 μg/mL inhibited MMP-9 secretion/activity in cultured fibroblasts after UVB exposure. In addition, IPE inhibited the phosphorylation of p38, ERK, and JNK induced by UVB. Furthermore, IPE inhibited the UVB-induced expression of Smad7. In addition, IPE at 1 μg/mL inhibited NO production and COX-2 expression in UV-exposed fibroblasts. These findings show that IPE exhibits anti-inflammatory and anti-photoaging activities, indicating that IPE could be a potential anti-aging agent.

摘要

具有高多酚含量的仪花表现出抗氧化活性,并减少 UVB 诱导的细胞内活性氧的产生。在这项研究中,光老化筛选实验的结果表明,IPE 在 1000μg/mL 时将细菌胶原酶的活性降低了 92.7±4.2%,将弹性蛋白酶的活性降低了 32.6±1.4%。因此,我们研究了 IPE 发挥其抗光老化活性的机制。IPE 在 1μg/mL 时导致 I 型前胶原表达增加,在 5μg/mL 时增加成纤维细胞中的总胶原合成。我们发现,IPE 在经 UV 照射(40mJ/cm²)的成纤维细胞中,在 1、5 和 10μg/mL 时分别抑制 MMP-1、MMP-3 和 MMP-9 的表达。明胶酶谱分析表明,IPE 在 50μg/mL 时抑制了经 UVB 暴露后的培养成纤维细胞中 MMP-9 的分泌/活性。此外,IPE 抑制了 UVB 诱导的 p38、ERK 和 JNK 的磷酸化。此外,IPE 抑制了 UVB 诱导的 Smad7 的表达。此外,IPE 在 1μg/mL 时抑制了经 UV 暴露的成纤维细胞中 NO 的产生和 COX-2 的表达。这些发现表明 IPE 具有抗炎和抗光老化活性,表明 IPE 可能是一种潜在的抗衰老剂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eae1/3235733/575d5fe85ac1/ECAM2012-417346.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eae1/3235733/613eca1b469a/ECAM2012-417346.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eae1/3235733/08d481ade8ec/ECAM2012-417346.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eae1/3235733/6bde3a02ced4/ECAM2012-417346.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eae1/3235733/5e7b6ca50574/ECAM2012-417346.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eae1/3235733/575d5fe85ac1/ECAM2012-417346.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eae1/3235733/613eca1b469a/ECAM2012-417346.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eae1/3235733/08d481ade8ec/ECAM2012-417346.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eae1/3235733/6bde3a02ced4/ECAM2012-417346.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eae1/3235733/5e7b6ca50574/ECAM2012-417346.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eae1/3235733/575d5fe85ac1/ECAM2012-417346.005.jpg

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