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      Drug Design, Development and Therapy (submit here)

      This international, peer-reviewed Open Access journal by Dove Medical Press focuses on the design and development of drugs, as well as the clinical outcomes, patient safety, and programs targeted at the effective and safe use of medicines. Sign up for email alerts here.

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      EGCG Regulates Cell Apoptosis of Human Umbilical Vein Endothelial Cells Grown on 316L Stainless Steel for Stent Implantation

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          Abstract

          Background

          Nowadays, medical grade 316L stainless steel (316L SS) is being widely used for intravascular stents, and the drug-eluting stent (DES) system is able to significantly reduce the occurrences of in-stent restenosis. But the drugs and the polymer coating used in DES potentially induce the forming of late stent thrombosis. In order to reduce the occurrence of ISR after stent implantation, the development of novel drugs for DESs is urgently needed.

          Methods

          This study aimed to investigate the potential mechanisms of epigallocatechin-3-gallate (EGCG) on human umbilical vein endothelial cells (HUVEC) grown on 316L stainless steel (316L SS) using flow cytometry and Q-PCR methods.

          Results

          Our results showed that EGCG (12.5, 25, 50, 100 μmol/L) significantly inhibited HUVEC proliferation. Flow cytometry analysis indicated that EGCG (25, 50, 100 μmol/L) induced apoptosis. Moreover, qRT-PCRrevealed that genes associated with cell apoptosis (caspase-3, 8, 9, Fas) and autophagy (Atg 5, Atg 7, Atg 12) were up-regulated after EGCG treatment.

          Conclusion

          These findings indicate that EGCG possesses chemo preventive potential in stent coating which may serve as a novel new drug for stent implantation.

          Most cited references29

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          The complexity of NF-κB signaling in inflammation and cancer

          Bastian Hoesel, Johannes A. Schmid (2013)
          The NF-κB family of transcription factors has an essential role in inflammation and innate immunity. Furthermore, NF-κB is increasingly recognized as a crucial player in many steps of cancer initiation and progression. During these latter processes NF-κB cooperates with multiple other signaling molecules and pathways. Prominent nodes of crosstalk are mediated by other transcription factors such as STAT3 and p53 or the ETS related gene ERG. These transcription factors either directly interact with NF-κB subunits or affect NF-κB target genes. Crosstalk can also occur through different kinases, such as GSK3-β, p38, or PI3K, which modulate NF-κB transcriptional activity or affect upstream signaling pathways. Other classes of molecules that act as nodes of crosstalk are reactive oxygen species and miRNAs. In this review, we provide an overview of the most relevant modes of crosstalk and cooperativity between NF-κB and other signaling molecules during inflammation and cancer.
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            Life and death partners: apoptosis, autophagy and the cross-talk between them.

            A Eisenberg-Lerner, S Bialik, H-U Simon … (2009)
            It is not surprising that the demise of a cell is a complex well-controlled process. Apoptosis, the first genetically programmed death process identified, has been extensively studied and its contribution to the pathogenesis of disease well documented. Yet, apoptosis does not function alone to determine a cell's fate. More recently, autophagy, a process in which de novo-formed membrane-enclosed vesicles engulf and consume cellular components, has been shown to engage in a complex interplay with apoptosis. In some cellular settings, it can serve as a cell survival pathway, suppressing apoptosis, and in others, it can lead to death itself, either in collaboration with apoptosis or as a back-up mechanism when the former is defective. The molecular regulators of both pathways are inter-connected; numerous death stimuli are capable of activating either pathway, and both pathways share several genes that are critical for their respective execution. The cross-talk between apoptosis and autophagy is therefore quite complex, and sometimes contradictory, but surely critical to the overall fate of the cell. Furthermore, the cross-talk is a key factor in the outcome of death-related pathologies such as cancer, its development and treatment.
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              Green tea catechin, epigallocatechin-3-gallate (EGCG): mechanisms, perspectives and clinical applications.

              Brahma Singh, Sharmila Shankar, Rakesh Srivastava (2011)
              An expanding body of preclinical evidence suggests EGCG, the major catechin found in green tea (Camellia sinensis), has the potential to impact a variety of human diseases. Apparently, EGCG functions as a powerful antioxidant, preventing oxidative damage in healthy cells, but also as an antiangiogenic and antitumor agent and as a modulator of tumor cell response to chemotherapy. Much of the cancer chemopreventive properties of green tea are mediated by EGCG that induces apoptosis and promotes cell growth arrest by altering the expression of cell cycle regulatory proteins, activating killer caspases, and suppressing oncogenic transcription factors and pluripotency maintain factors. In vitro studies have demonstrated that EGCG blocks carcinogenesis by affecting a wide array of signal transduction pathways including JAK/STAT, MAPK, PI3K/AKT, Wnt and Notch. EGCG stimulates telomere fragmentation through inhibiting telomerase activity. Various clinical studies have revealed that treatment by EGCG inhibits tumor incidence and multiplicity in different organ sites such as liver, stomach, skin, lung, mammary gland and colon. Recent work demonstrated that EGCG reduced DNMTs, proteases, and DHFR activities, which would affect transcription of TSGs and protein synthesis. EGCG has great potential in cancer prevention because of its safety, low cost and bioavailability. In this review, we discuss its cancer preventive properties and its mechanism of action at numerous points regulating cancer cell growth, survival, angiogenesis and metastasis. Therefore, non-toxic natural agent could be useful either alone or in combination with conventional therapeutics for the prevention of tumor progression and/or treatment of human malignancies. Copyright © 2011 Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Drug Des Devel Ther
                Journal ID (iso-abbrev): Drug Des Devel Ther
                Journal ID (publisher-id): dddt
                Journal ID (pmc): dddt
                Title: Drug Design, Development and Therapy
                Publisher: Dove
                ISSN (Electronic): 1177-8881
                Publication date (Electronic): 11 February 2021
                Publication date Collection: 2021
                Volume: 15
                Pages: 493-499
                Affiliations
                [1 ]Department of Cardiology, The Second Hospital of Jilin University , Changchun, 130041, People’s Republic of China
                [2 ]Department of Nutrition and Food Hygiene, School of Public Health, Jilin University , Changchun, 130021, People’s Republic of China
                [3 ]Department of Physiology, College of Basic Medical Sciences, Jilin University , Changchun, 130021, People’s Republic of China
                [4 ]Jilin Engineering Research Center of Public Health Detection , Changchun, 130021, People’s Republic of China
                Author notes
                Correspondence: Kun Xu Department of Nutrition and Food Hygiene, School of Public Health, Jilin University , Changchun, 130021, People’s Republic of China Email xukun@jlu.edu.cn
                Author information
                http://orcid.org/0000-0002-1475-9910
                Article
                Publisher ID: 296548
                DOI: 10.2147/DDDT.S296548
                PMC ID: 7886104
                SO-VID: fd8ea08b-857d-46d2-b460-a11204c61e08
                Copyright © © 2021 Wang et al.
                License:

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                Date received : 09 December 2020
                Date accepted : 21 January 2021
                Page count
                Figures: 3, Tables: 1, References: 29, Pages: 7
                Categories
                Subject: Original Research

                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: egcg,316 stainless steel,huvecs,apoptosis
                Data availability:
                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: egcg, 316 stainless steel, huvecs, apoptosis

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