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UVB 照射皮肤角质细胞中可食用淡水藻类的抗细胞凋亡和抗炎活性。

Anti-Apoptotic and Anti-Inflammatory Activities of Edible Fresh Water Algae in UVB-Irradiated Skin Keratinocytes.

机构信息

Department of Integrative Biotechnology, Sungkyunkwan University, Suwon 16419, Republic of Korea.

Department of Pharmaceutical and Biomedical Engineering, Cheongju University, Cheongju 28503, Republic of Korea.

出版信息

Am J Chin Med. 2019;47(8):1853-1868. doi: 10.1142/S0192415X19500940. Epub 2019 Dec 2.

DOI:10.1142/S0192415X19500940
PMID:31786945
Abstract

Skin is the outer tissue layer and is a barrier protecting the body from various external stresses. The fresh water green edible algae has antiviral, antimicrobial, and anti-inflammatory properties; however, few studies of its effects on skin-protection have been reported. In this study, ethanol extract (Pj-EE) was prepared, and its skin-protective properties were investigated in skin keratinocytes. Pj-EE inhibited ROS production in UVB-irradiated HaCaT cells without cytotoxicity. Pj-EE also suppressed the apoptotic death of UVB-irradiated HaCaT cells by decreasing the generation of apoptotic bodies and the proteolytic activation of apoptosis caspase-3, -8, and -9. Moreover, Pj-EE downregulated the mRNA expression of the inflammatory gene cyclooxygenase-2 (COX-2), the pro-inflammatory cytokine genes interleukin (IL)-1, IL-8, IL-6, tumor necrosis factor (TNF)-, and interferon (IFN)-, and the tissue remodeling genes matrix metalloproteinase (MMP)-1, -2, -3, and -9. The Pj-EE-induced anti-inflammatory effect was mediated by suppressing the activation of nuclear factor-kappa B (NF-B) signaling pathway in the UVB-irradiated HaCaT cells. Taken together, these results suggest that Pj-EE exerts skin-protective effects through anti-oxidant, anti-apoptotic, and anti-inflammatory activities in skin keratinocytes.

摘要

皮肤是外层组织,是保护身体免受各种外部压力的屏障。淡水绿食用藻类具有抗病毒、抗菌和抗炎特性;然而,关于其对皮肤保护作用的研究很少。本研究制备了乙醇提取物(Pj-EE),并在皮肤角质形成细胞中研究了其皮肤保护特性。Pj-EE 抑制了 UVB 照射的 HaCaT 细胞中 ROS 的产生,而没有细胞毒性。Pj-EE 还通过减少凋亡小体的产生和凋亡半胱天冬酶-3、-8 和-9 的蛋白水解激活来抑制 UVB 照射的 HaCaT 细胞的凋亡死亡。此外,Pj-EE 下调了炎症基因环氧合酶-2 (COX-2)、促炎细胞因子基因白细胞介素 (IL)-1、IL-8、IL-6、肿瘤坏死因子 (TNF)-和干扰素 (IFN)-以及组织重塑基因基质金属蛋白酶 (MMP)-1、-2、-3 和-9 的 mRNA 表达。Pj-EE 诱导的抗炎作用是通过抑制 NF-B 信号通路在 UVB 照射的 HaCaT 细胞中的激活来介导的。综上所述,这些结果表明 Pj-EE 通过在皮肤角质形成细胞中发挥抗氧化、抗凋亡和抗炎作用来发挥皮肤保护作用。

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