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没食子酸表没食子儿茶素酯对血红素合成途径和原卟啉 IX 生成的体外影响。

In Vitro Effect of Epigallocatechin Gallate on Heme Synthesis Pathway and Protoporphyrin IX Production.

机构信息

Laboratory of Integrative Biology (LIBi), Centro de Excelencia en Medicina Traslacional (CEMT), Scientific and Technological Bioresource Nucleus (BIOREN), Universidad de La Frontera, Temuco 4780000, Chile.

Millennium Institute of Immunology and Immunotherapy, Santiago 8320165, Chile.

出版信息

Int J Mol Sci. 2024 Aug 9;25(16):8683. doi: 10.3390/ijms25168683.

DOI:10.3390/ijms25168683
PMID:39201369
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11354225/
Abstract

Photodynamic therapy (PDT) treats nonmelanoma skin cancer. PDT kills cells through reactive oxygen species (ROS), generated by interaction among cellular O photosensitizer and specific light. Protoporphyrin IX (PpIX) is a photosensitizer produced from methyl aminolevulinate (MAL) by heme group synthesis (HGS) pathway. In PDT-resistant cells, PDT efficacy has been improved by addition of epigallocatechin gallate (EGCG). Therefore, the aim of this work is to evaluate the effect of EGCG properties over MAL-TFD and PpIX production on A-431 cell line. EGCG's role over cell proliferation (flow cytometry and wound healing assay) and clonogenic capability (clonogenic assay) was evaluated in A-431 cell line, while the effect of EGCG over MAL-PDT was determined by cell viability assay (MTT), PpIX and ROS detection (flow cytometry), intracellular iron quantification and gene expression of HGS enzymes (RT-qPCR). Low concentrations of EGCG (<50 µM) did not have an antiproliferative effect over A-431 cells; however, EGCG inhibited clonogenic cell capability. Furthermore, EGCG (<50 µM) improved MAL-PDT cytotoxicity, increasing PpIX and ROS levels, exerting a positive influence on PpIX synthesis, decreasing intracellular iron concentration and modifying HGS enzyme gene expression such as (upregulated) and (downregulated). EGCG inhibits clonogenic capability and modulates PpIX synthesis, enhancing PDT efficacy in resistant cells.

摘要

光动力疗法 (PDT) 用于治疗非黑色素瘤皮肤癌。PDT 通过细胞内 O 光敏剂与特定光之间的相互作用产生的活性氧物种 (ROS) 杀死细胞。原卟啉 IX (PpIX) 是由甲羟戊酸 (MAL) 通过血红素合成 (HGS) 途径产生的光敏剂。在 PDT 耐药细胞中，通过添加表没食子儿茶素没食子酸酯 (EGCG) 可以提高 PDT 的疗效。因此，本工作旨在评估 EGCG 对 MAL-TFD 和 PpIX 生成的特性对 A-431 细胞系的影响。在 A-431 细胞系中评估 EGCG 对细胞增殖（流式细胞术和划痕愈合试验）和集落形成能力（集落形成试验）的作用，以及通过细胞活力测定（MTT）、PpIX 和 ROS 检测（流式细胞术）、细胞内铁定量和 HGS 酶基因表达（RT-qPCR）确定 EGCG 对 MAL-PDT 的影响。低浓度的 EGCG（<50µM）对 A-431 细胞没有增殖抑制作用；然而，EGCG 抑制了集落形成细胞的能力。此外，EGCG（<50µM）提高了 MAL-PDT 的细胞毒性，增加了 PpIX 和 ROS 水平，对 PpIX 合成产生了积极影响，降低了细胞内铁浓度，并改变了 HGS 酶基因表达，如 （上调）和 （下调）。EGCG 抑制集落形成能力并调节 PpIX 合成，增强耐药细胞中 PDT 的疗效。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f6a/11354225/71281f1c0247/ijms-25-08683-g009.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f6a/11354225/c7496cad0da1/ijms-25-08683-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f6a/11354225/6bd913641787/ijms-25-08683-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f6a/11354225/71281f1c0247/ijms-25-08683-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f6a/11354225/1b872b30a371/ijms-25-08683-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f6a/11354225/9038e619488c/ijms-25-08683-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f6a/11354225/f994f208c18d/ijms-25-08683-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f6a/11354225/14f15f2d74c9/ijms-25-08683-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f6a/11354225/26699500b920/ijms-25-08683-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f6a/11354225/5da879cb9a3e/ijms-25-08683-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f6a/11354225/c7496cad0da1/ijms-25-08683-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f6a/11354225/6bd913641787/ijms-25-08683-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f6a/11354225/71281f1c0247/ijms-25-08683-g009.jpg

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