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首页> 外文期刊>The Korean Journal of Physiology & Pharmacology >p-Coumaric Acid Attenuates UVB-Induced Release of Stratifin from Keratinocytes and Indirectly Regulates Matrix Metalloproteinase 1 Release from Fibroblasts
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p-Coumaric Acid Attenuates UVB-Induced Release of Stratifin from Keratinocytes and Indirectly Regulates Matrix Metalloproteinase 1 Release from Fibroblasts

机译：对香豆酸减弱了紫外线诱导的角质形成细胞释放Stratifin并间接调节成纤维细胞释放的基质金属蛋白酶1。

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摘要

Ultraviolet (UV) radiation-induced loss of dermal extracellular matrix is associated with skin photoaging. Recent studies demonstrated that keratinocyte-releasable stratifin (SFN) plays a critical role in skin collagen metabolism by inducing matrix metalloproteinase 1 (MMP1) expression in target fibroblasts. In the present study, we examined whether SFN released from UVB-irradiated epidermal keratinocytes increases MMP1 release from dermal fibroblasts, and whether these events are affected by p-coumaric acid (p-CA), a natural phenolic compound with UVB-shielding and antioxidant properties. HaCaT cells were exposed to UVB in the absence and presence of p-CA, and the conditioned medium was used to stimulate fibroblasts in medium transfer experiments. The cells and media were analyzed to determine the expressions/releases of SFN and MMP1. UVB exposure increased SFN release from keratinocytes into the medium. The conditioned medium of UVB-irradiated keratinocytes increased MMP1 release from fibroblasts. The depletion of SFN using a siRNA rendered the conditioned medium of UVB-irradiated keratinocytes ineffective at stimulating fibroblasts to release MMP1. p-CA mitigated UVB-induced SFN expression in keratinocytes, and attenuated the MMP1 release by fibroblasts in medium transfer experiments. In conclusion, the present study demonstrated that the use of UV absorbers such as p-CA would reduce UV-induced SFN-centered signaling events involved in skin photoaging.
机译：紫外线（UV）引起的真皮细胞外基质损失与皮肤光老化有关。最近的研究表明，可释放角质形成细胞的层状素（SFN）在皮肤胶原蛋白代谢中起着至关重要的作用，方法是诱导目标成纤维细胞中的基质金属蛋白酶1（MMP1）表达。在本研究中，我们检查了从UVB照射的表皮角质形成细胞释放的SFN是否增加了从皮肤成纤维细胞释放的MMP1，以及这些事件是否受到对香豆酸（p-CA）的影响，对香豆酸（p-CA）是具有UVB屏蔽和抗氧化剂的天然酚类化合物属性。在不存在和存在p-CA的情况下，将HaCaT细胞暴露于UVB中，并在培养基转移实验中将条件培养基用于刺激成纤维细胞。分析细胞和培养基以确定SFN和MMP1的表达/释放。 UVB暴露会增加SFN从角质形成细胞向培养基的释放。 UVB照射的角质形成细胞的条件培养基增加了MMP1从成纤维细胞的释放。使用siRNA耗尽SFN使得UVB照射的角质形成细胞的条件培养基不能有效刺激成纤维细胞释放MMP1。在培养基转移实验中，p-CA减轻了UVB诱导的角质形成细胞中SFN的表达，并减弱了成纤维细胞释放的MMP1。总而言之，本研究表明使用紫外线吸收剂（例如p-CA）将减少紫外线引起的皮肤光老化所涉及的以SFN为中心的信号事件。

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