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藻蓝蛋白通过 PKCα/βⅡ-Nrf-2/HO-1 依赖性通路在人原代皮肤细胞中保护细胞免受 UVB 诱导的细胞凋亡。

Phycocyanin Protects Against UVB-induced Apoptosis Through the PKC α/βII-Nrf-2/HO-1 Dependent Pathway in Human Primary Skin Cells.

机构信息

KM Convergence Research Division, Korea Institute of Oriental Medicine, 1672 Yuseong-daero, Yuseong-gu, Daejeon 34054, Korea.

Department of Korean Life Science and Technology, Korea University of Science and Technology, Daejeon 34113, Korea.

出版信息

Molecules. 2018 Feb 22;23(2):478. doi: 10.3390/molecules23020478.

DOI:10.3390/molecules23020478
PMID:29470442
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6017183/
Abstract

Phycocyanin (Pc) is one of the active pigment constituents of microalgae. It has been used for its potent antioxidant and anti-inflammatory properties. However, the protective effects of Pc against ultraviolet-B (UVB)-induced primary skin cells damage are still undefined. In the present study, we investigated whether Pc prevented UVB-induced apoptotic cell death in human dermal fibroblasts (HDF) and human epidermal keratinocytes (HEK). Pc induced the transcription of heme oxygenase-1 (HO-1). Furthermore, Pc treatments resulted in a marked increase in nuclear factor erythroid-derived 2 (NF-E2)-like 2 (Nrf-2) nuclear translocation. Also, Pc protected UVB induced apoptosis and reduced the p53 and Bax levels, as well as caspase-3 activation. Pc treatment showed a significantly enhanced effect on the phosphorylation of protein kinase C (PKC) α/β II, but not that of p38 mitogen-activated protein kinase (MAPK) or Akt. Induction of HO-1 induced by Pc was suppressed by Go6976, a selective inhibitor of PKC α/β II. In addition, knockdown of HO-1 by small interfering (siRNA) caused a significant increase in poly (ADP-ribose) polymerase 1 (PARP-1) cleavage and caspase-3 activation after Pc pretreatment. Taken together, our results demonstrate that Pc-induced expression of HO-1 is mediated by the PKC α/β II-Nrf-2/HO-1 pathway, and inhibits UVB-induced apoptotic cell death in primary skin cells.

摘要

藻蓝蛋白 (Pc) 是微藻中一种具有活性的色素成分。它具有很强的抗氧化和抗炎特性，因此被广泛应用。然而，Pc 对紫外线 B (UVB) 诱导的皮肤细胞损伤的保护作用仍未得到明确界定。在本研究中，我们研究了 Pc 是否可以预防人皮肤成纤维细胞 (HDF) 和人表皮角质形成细胞 (HEK) 中 UVB 诱导的细胞凋亡。Pc 诱导血红素加氧酶-1 (HO-1) 的转录。此外，Pc 处理导致核因子红细胞衍生 2 (NF-E2)-样 2 (Nrf-2) 核易位显著增加。Pc 还可以保护 UVB 诱导的细胞凋亡，并降低 p53 和 Bax 水平，同时抑制半胱氨酸天冬氨酸蛋白酶-3 (caspase-3) 的激活。Pc 处理对蛋白激酶 C (PKC) α/β II 的磷酸化有明显的增强作用，但对丝裂原活化蛋白激酶 (MAPK) p38 或 Akt 的磷酸化没有影响。Pc 诱导的 HO-1 诱导作用被 PKC α/β II 的选择性抑制剂 Go6976 抑制。此外，用小干扰 RNA (siRNA) 敲低 HO-1 后，Pc 预处理会导致多聚 (ADP-核糖) 聚合酶 1 (PARP-1) 切割和 caspase-3 激活显著增加。综上所述，我们的结果表明，Pc 诱导的 HO-1 表达是通过 PKC α/β II-Nrf-2/HO-1 通路介导的，并抑制原代皮肤细胞中 UVB 诱导的细胞凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d20f/6017183/cb268c888aa7/molecules-23-00478-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d20f/6017183/d9d47352909a/molecules-23-00478-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d20f/6017183/f03d5c38a743/molecules-23-00478-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d20f/6017183/171172e51c27/molecules-23-00478-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d20f/6017183/32988776988d/molecules-23-00478-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d20f/6017183/cb268c888aa7/molecules-23-00478-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d20f/6017183/d9d47352909a/molecules-23-00478-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d20f/6017183/f03d5c38a743/molecules-23-00478-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d20f/6017183/171172e51c27/molecules-23-00478-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d20f/6017183/32988776988d/molecules-23-00478-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d20f/6017183/cb268c888aa7/molecules-23-00478-g005.jpg

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