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通过抑制MAPK/AP-1/MMP-1信号通路对紫外线B诱导的光老化的防护作用

Protection against UVB-Induced Photoaging by via Inhibition of MAPK/AP-1/MMP-1 Signaling.

作者信息

Choi Hee-Jeong, Alam Md Badrul, Baek Mi-Eun, Kwon Yoon-Gyung, Lim Ji-Young, Lee Sang-Han

机构信息

Department of Food Science And Biotechnology, Graduate School, Kyungpook National University, Daegu 41566, Republic of Korea.

Food and Bio-Industry Research Institute, Inner Beauty/Antiaging Center, Kyungpook National University, Daegu 41566, Republic of Korea.

出版信息

Oxid Med Cell Longev. 2020 Jun 22;2020:2905362. doi: 10.1155/2020/2905362. eCollection 2020.

DOI:10.1155/2020/2905362
PMID:32685089
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7330638/
Abstract

Ultraviolet B (UVB) irradiation is major causative factor in skin aging. The aim of the present study was to investigate the protective effect of a 50% ethanol extract from (NF50E) against UVB-induced skin aging. The results indicated that NF50E exerted potent antioxidant activity (IC = 17.55 ± 1.63 and 10.78 ± 0.63 g/mL for DPPH and ABTS-radical scavenging activity, respectively) in a dose-dependent manner. High-performance liquid chromatography revealed that pengxianencin A, protocatechuic acid, catechin, chlorogenic acid, epicatechin, and kaempferol were components of the extract. In addition, the extract exhibited elastase inhibitory activity (IC = 17.96 ± 0.39 g/mL). NF50E protected against UVB-induced HaCaT cell death and strongly suppressed UVB-stimulated cellular reactive oxygen species generation without cellular toxicity. Moreover, topical application of NF50E mitigated UVB-induced photoaging lesions including skin erythema and skin thickness in BALB/C mice. NF50E treatment inhibited UVB-induced collagen degradation as well as MMP-1 and IL-1 expressions and significantly stimulated SIRT1 expression. Furthermore, the extract treatment markedly suppressed the activation of NF-B and AP-1 (p-c-Jun) by deactivating the p38 and JNK proteins. Taken together, current data suggest that NF50E exhibits potent antioxidant potential and protection against photoaging by attenuating MMP-1 activity and collagen degradation possibly through the downregulation of MAPK/NF-B/AP-1 signaling and SIRT1 activation.

摘要

紫外线B(UVB)照射是皮肤衰老的主要致病因素。本研究的目的是探讨[具体植物名称]50%乙醇提取物(NF50E)对UVB诱导的皮肤衰老的保护作用。结果表明,NF50E以剂量依赖的方式发挥强大的抗氧化活性(DPPH和ABTS自由基清除活性的IC50分别为17.55±1.63和10.78±0.63μg/mL)。高效液相色谱显示,彭县霉素A、原儿茶酸、儿茶素、绿原酸、表儿茶素和山奈酚是该提取物的成分。此外,该提取物表现出弹性蛋白酶抑制活性(IC50=17.96±0.39μg/mL)。NF50E可保护HaCaT细胞免受UVB诱导的死亡,并强烈抑制UVB刺激的细胞活性氧生成,且无细胞毒性。此外,在BALB/C小鼠中局部应用NF50E可减轻UVB诱导的光老化损伤,包括皮肤红斑和皮肤厚度。NF50E处理可抑制UVB诱导的胶原蛋白降解以及MMP-1和IL-1的表达,并显著刺激SIRT1的表达。此外,提取物处理通过使p38和JNK蛋白失活,显著抑制了NF-κB和AP-1(p-c-Jun)的激活。综上所述,目前的数据表明,NF50E具有强大的抗氧化潜力,并通过下调MAPK/NF-κB/AP-1信号通路和激活SIRT1,可能通过减弱MMP-1活性和胶原蛋白降解来保护皮肤免受光老化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b028/7330638/dd66062da76e/OMCL2020-2905362.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b028/7330638/96da23c6f7a1/OMCL2020-2905362.001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b028/7330638/6fc8e1c7a57f/OMCL2020-2905362.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b028/7330638/dd66062da76e/OMCL2020-2905362.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b028/7330638/96da23c6f7a1/OMCL2020-2905362.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b028/7330638/0be1e64e49e7/OMCL2020-2905362.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b028/7330638/cb826ac3fe7a/OMCL2020-2905362.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b028/7330638/4ae18f979df2/OMCL2020-2905362.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b028/7330638/30e519087b33/OMCL2020-2905362.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b028/7330638/f2e9f5cc0bb6/OMCL2020-2905362.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b028/7330638/6fc8e1c7a57f/OMCL2020-2905362.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b028/7330638/dd66062da76e/OMCL2020-2905362.008.jpg

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