低剂量 ALA-PDT 对 UVA 照射诱导的成纤维细胞光老化的影响及作用机制。

Effects of low-dose ALA-PDT on fibroblast photoaging induced by UVA irradiation and the underlying mechanisms.

机构信息

Department of Dermatology, Daping Hospital, The Army Medical University, Chongqing, 400042, China.

Key Laboratory of Biorheological Science and Technology, Ministry of Education; Chongqing University, Chongqing, 400044, China.

出版信息

Photodiagnosis Photodyn Ther. 2019 Sep;27:79-84. doi: 10.1016/j.pdpdt.2019.05.006. Epub 2019 May 7.

DOI:10.1016/j.pdpdt.2019.05.006

PMID:31075320

Abstract

OBJECTIVES

To investigate the effects of low-dose aminolevulinic acid photodynamic therapy (ALA-PDT) on photoaging in human dermal fibroblasts (HDFs) and to explore the mechanism of Nuclear factor erythroid 2-related factor 2(Nrf2)-mediated photorejuvenation in vitro.

METHODS

A photoaging model was established through repeated exposure of HDFs to UVA. Total superoxide dismutase (SOD) expression was detected by a SOD activity assay. Nrf2 was knocked down through adenovirus infection, and successful knockdown was confirmed by Western blot analysis and quantitative polymerase chain reaction.

RESULTS

Sustained exposure to UVA induced photoaging in HDFs. Total SOD activity was significantly increased by low-dose aminolevulinic acid (ALA)-PDT. Upon application of low doses of ALA-PDT to photoaging HDFs, Nrf2 was translocated to the nucleus; in addition, the expression of Nrf2, transforming growth factor-β1 (TGF-β1), type I and III collagen (COL1 and COL3), heme oxygenase 1 (HO-1), and p-ERK was increased, while the expression of matrix metalloproteinase 9 (MMP-9) was decreased. However, after Nrf2 was knocked down in HDFs, the expression of TGF-β1, COL1, COL3, and HO-1 was significantly decreased, while the expression of MMP-9 was increased.

CONCLUSION

This study revealed that low-dose ALA-PDT decreases UVA-mediated photoaging through an Nrf2-mediated antioxidant effect.

摘要

目的

研究低浓度氨基酮戊酸光动力疗法（ALA-PDT）对人真皮成纤维细胞（HDF）光老化的影响，并探讨体外核因子红细胞 2 相关因子 2（Nrf2）介导光老化的机制。

方法

通过重复暴露于 UVA 建立 HDF 光老化模型。通过 SOD 活性测定检测总超氧化物歧化酶（SOD）的表达。通过腺病毒感染敲低 Nrf2，并通过 Western blot 分析和定量聚合酶链反应确认成功敲低。

结果

持续暴露于 UVA 可诱导 HDF 光老化。低浓度氨基酮戊酸（ALA）-PDT 可显著增加总 SOD 活性。在将低剂量 ALA-PDT 应用于光老化 HDF 时，Nrf2 易位到核内；此外，Nrf2、转化生长因子-β1（TGF-β1）、I 型和 III 型胶原（COL1 和 COL3）、血红素加氧酶 1（HO-1）和 p-ERK 的表达增加，而基质金属蛋白酶 9（MMP-9）的表达减少。然而，在 HDF 中敲低 Nrf2 后，TGF-β1、COL1、COL3 和 HO-1 的表达显著减少，而 MMP-9 的表达增加。