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以 SDF-1 为靶点,利用长松萝提取物解决皮肤色素沉着问题的有效策略。

Targeting SDF-1 as an efficient strategy to resolve skin hyperpigmentation issues with Himanthalia elongata extract.

机构信息

Research & Development, Givaudan Active Beauty, Pomacle, France.

Research & Development, Givaudan Active Beauty, Ile-Grande, France.

出版信息

J Cosmet Dermatol. 2023 Feb;22(2):383-394. doi: 10.1111/jocd.15357. Epub 2022 Sep 16.

DOI:10.1111/jocd.15357
PMID:36062379
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10087502/
Abstract

BACKGROUND

During aging, human skin is facing hyperpigmentation disorders: senile lentigo (chronobiologic aging) leads to loss of melanogenesis' control while solar lentigo (UV exposure) promotes an increase of oxidized proteins, melanogenesis, and lipofuscin.

AIMS

Stromal-cell-derived-factor-1 (SDF-1) was identified as key regulator of hyperpigmentation and its expression is reduced in senescent fibroblasts, highlighting this protein as new target for skin hyperpigmentation.

MATERIALS

We developed two skin explant models mimicking of senile and solar lentigo, based on H O systemic treatment and UV irradiation, respectively. We evaluated Himanthalia elongata extract (HEX) on these models after 5 days of treatment and analyzed SDF-1 expression and skin pigmentation. For solar lentigo, we also analyzed oxidized proteins and lipofuscin accumulation. Finally, we evaluated HEX in vivo on nearly 100 multi ethnicities' volunteers.

RESULTS

SDF-1 expression decreased in senile lentigo model, associated with hyperpigmentation. HEX application restored SDF-1 expression, leading to skin pigmentation decrease. For solar lentigo, we showed an impact of UVs on SDF-1 expression linked to hyperpigmentation, while the application of HEX restored SDF-1 expression and reduced skin pigmentation. On same model, HEX reduced oxidized proteins quantity and lipofuscin which increased after UV exposure. Clinically, HEX reduced dark spot pigmentation on Caucasian volunteers' hands and on Asian and African volunteers' face after 28 days.

DISCUSSION

We have developed ex vivo models mimetic of senile and solar lentigo and showed for a very first time that SDF-1 can be also a key regulator for UV-induced hyperpigmentation.

CONCLUSION

Our ex vivo and clinical studies highlighted the power of HEX with strong reduction of dark spots regardless of volunteers' ethnicities.

摘要

背景

随着年龄的增长,人类皮肤会出现色素沉着紊乱:老年斑(生物钟衰老)导致黑色素生成失去控制,而太阳斑(紫外线暴露)则促进氧化蛋白、黑色素生成和脂褐素的增加。

目的

基质细胞衍生因子-1(SDF-1)被鉴定为色素沉着的关键调节剂,其在衰老成纤维细胞中的表达减少,突出了这种蛋白质作为皮肤色素沉着的新靶标。

材料

我们开发了两种皮肤外植体模型,分别模拟老年斑和太阳斑,基于 H O 全身治疗和紫外线照射。我们在治疗 5 天后评估了 Himanthalia elongata 提取物(HEX)对这些模型的影响,并分析了 SDF-1 的表达和皮肤色素沉着。对于太阳斑,我们还分析了氧化蛋白和脂褐素的积累。最后,我们在近 100 名多民族志愿者中评估了 HEX 的体内作用。

结果

老年斑模型中 SDF-1 的表达减少,与色素沉着有关。HEX 的应用恢复了 SDF-1 的表达,导致皮肤色素沉着减少。对于太阳斑,我们显示了紫外线对 SDF-1 表达的影响与色素沉着有关,而 HEX 的应用恢复了 SDF-1 的表达并减少了皮肤色素沉着。在同一模型上,HEX 减少了紫外线暴露后增加的氧化蛋白数量和脂褐素。临床上,HEX 减少了白种人志愿者手部、亚洲和非洲志愿者面部的黑斑色素沉着,在 28 天后。

讨论

我们开发了模拟老年斑和太阳斑的体外模型,并首次表明 SDF-1 也可能是紫外线诱导色素沉着的关键调节剂。

结论

我们的体外和临床研究强调了 HEX 的强大功效,可以减少无论志愿者种族如何的黑斑。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ea/10087502/f2760fa8176a/JOCD-22-383-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ea/10087502/9802c25cfe0c/JOCD-22-383-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ea/10087502/90cdad562e84/JOCD-22-383-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ea/10087502/48613f4bd6c9/JOCD-22-383-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ea/10087502/f813dbe3a834/JOCD-22-383-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ea/10087502/40b19befec68/JOCD-22-383-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ea/10087502/c203bd8bc92b/JOCD-22-383-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ea/10087502/a4337f060caa/JOCD-22-383-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ea/10087502/6c1b385a4451/JOCD-22-383-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ea/10087502/f2760fa8176a/JOCD-22-383-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ea/10087502/9802c25cfe0c/JOCD-22-383-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ea/10087502/90cdad562e84/JOCD-22-383-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ea/10087502/48613f4bd6c9/JOCD-22-383-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ea/10087502/f813dbe3a834/JOCD-22-383-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ea/10087502/40b19befec68/JOCD-22-383-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ea/10087502/c203bd8bc92b/JOCD-22-383-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ea/10087502/a4337f060caa/JOCD-22-383-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ea/10087502/6c1b385a4451/JOCD-22-383-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ea/10087502/f2760fa8176a/JOCD-22-383-g001.jpg

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