Protective effects and mechanisms of  Terminalia catappa  L. methenolic extract on hydrogen-peroxide-induced oxidative stress in human skin fibroblasts

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Abstract

Background

Oxidative stress plays a crucial role in aging-related phenomenon, including skin aging and photoaging. This study investigated the protective role and possible mechanism of Terminalia catappa L. methanolic extract (TCE) in human fibroblasts (Hs68) against hydrogen peroxide (H ₂O ₂)-induced oxidative damage.

Methods

Various in vitro antioxidant assays were performed in this study. The effect and mechanisms of TCE on oxidative stress-induced oxidative damage were studied by using western blotting.

Results

The IC ₅₀ of TCE was 8.2 μg/mL for 1,1-diphenyl-2-picrylhydrazyl radical scavenging, 20.7 μg/mL for superoxide anion radical scavenging, 173.0 μg/mL for H ₂O ₂ scavenging, 44.8 μg/mL for hydroxyl radical scavenging, and 427.6 μg/mL for ferrous chelation activities. Moreover, TCE inhibited the H ₂O ₂-induced mitogen-activated protein kinase signaling pathway, resulting in the inhibition of c-Jun, c-Fos, matrix metalloproteinase (MMP)-1, MMP-3, MMP-9, and cyclooxygenase-2 expression. TCE also increased hemeoxygenase-1 expression inhibited by H ₂O ₂. Finally, TCE was demonstrated reverse type I procollagen expression in fibroblasts after H ₂O ₂ treatment.

Conclusions

According to our findings, TCE is a potent antioxidant and protective agent that can be used in antioxidative stress-induced skin aging.

Electronic supplementary material

The online version of this article (10.1186/s12906-018-2308-4) contains supplementary material, which is available to authorized users.

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Most cited references 31

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Prevention of cytotoxicity and inhibition of intercellular communication by antioxidant catechins isolated from Chinese green tea.

R Ruch, S. Cheng, J E Klaunig (1989)

An antioxidant fraction of Chinese green tea (green tea antioxidant; GTA), containing several catechins, has been previously shown to inhibit 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced tumor promotion in mouse skin. In the present study, GTA was shown to have antioxidative activity toward hydrogen peroxide (H2O2) and the superoxide radical (O2-). GTA also prevented oxygen radical and H2O2-induced cytotoxicity and inhibition of intercellular communication in cultured B6C3F1 mouse hepatocytes and human keratinocytes (NHEK cells). GTA (0.05-50 micrograms/ml) prevented the killing of hepatocytes (measured by lactate dehydrogenase release) by paraquat (1-10 mM) and glucose oxidase (0.8-40 micrograms/ml) in a concentration-dependent fashion. GTA (50 micrograms/ml) also prevented the inhibition of hepatocyte intercellular communication by paraquat (5 mM), glucose oxidase (0.8 micrograms/ml), and phenobarbital (500 micrograms/ml). In addition, GTA (50 micrograms/ml) prevented the inhibition of intercellular communication in human keratinocytes by TPA (100 ng/ml). Cytotoxicity and inhibition of intercellular communication, two possible mechanisms by which tumor promoters may produce their promoting effects were therefore prevented by GTA. The inhibition of these two effects of pro-oxidant compounds may suggest a mechanism by which GTA inhibits tumor promotion in vivo.

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Pathophysiology of premature skin aging induced by ultraviolet light.

G Fisher, Z. Wang, S Datta … (1997)

Long-term exposure to ultraviolet irradiation from sunlight causes premature skin aging (photoaging), characterized in part by wrinkles, altered pigmentation, and loss of skin tone. Photoaged skin displays prominent alterations in the collagenous extracellular matrix of connective tissue. We investigated the role of matrix-degrading metalloproteinases, a family of proteolytic enzymes, as mediators of collagen damage in photoaging. We studied 59 whites (33 men and 26 women, ranging in age from 21 to 58 years) with light-to-moderate skin pigmentation, none of whom had current or prior skin disease. Only some of the participants were included in each of the studies. We irradiated their buttock skin with fluorescent ultraviolet lights under standard conditions and obtained skin samples from irradiated and nonirradiated areas by keratome or punch biopsy. In some studies, tretinoin and its vehicle were applied to skin under occlusion 48 hours before ultraviolet irradiation. The expression of matrix metalloproteinases was determined by in situ hybridization, immunohistology, and in situ zymography. Irradiation-induced degradation of skin collagen was measured by radioimmunoassay of soluble cross-linked telopeptides. The protein level of tissue inhibitor of matrix metalloproteinases type 1 was determined by Western blot analysis. A single exposure to ultraviolet irradiation increased the expression of three matrix metalloproteinases -- collagenase, a 92-kd gelatinase, and stromelysin -- in skin connective tissue and outer skin layers, as compared with nonirradiated skin. The degradation of endogenous type I collagen fibrils was increased by 58 percent in irradiated skin, as compared with nonirradiated skin. Collagenase and gelatinase activity remained maximally elevated (4.4 and 2.3 times, respectively) for seven days with four exposures to ultraviolet irradiation, delivered at two-day intervals, as compared with base-line levels. Pretreatment of skin with tretinoin (all-trans-retinoic acid) inhibited the induction of matrix metalloproteinase proteins and activity (by 70 to 80 percent) in both connective tissue and outer layers of irradiated skin. Ultraviolet irradiation also induced tissue inhibitor of matrix metalloproteinases-1, which regulates the enzyme. Induction of the inhibitor was not affected by tretinoin. Multiple exposures to ultraviolet irradiation lead to sustained elevations of matrix metalloproteinases that degrade skin collagen and may contribute to photoaging. Treatment with topical tretinoin inhibits irradiation-induced matrix metalloproteinases but not their endogenous inhibitor.

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Mechanisms of Photoaging and Cutaneous Photocarcinogenesis, and Photoprotective Strategies with Phytochemicals

Ricardo Bosch, Neena Philips, Jorge A Suárez-Pérez … (2015)

Photoaging and photocarcinogenesis are primarily due to solar ultraviolet (UV) radiation, which alters DNA, cellular antioxidant balance, signal transduction pathways, immunology, and the extracellular matrix (ECM). The DNA alterations include UV radiation induced thymine-thymine dimers and loss of tumor suppressor gene p53. UV radiation reduces cellular antioxidant status by generating reactive oxygen species (ROS), and the resultant oxidative stress alters signal transduction pathways such as the mitogen-activated protein kinase (MAPK), the nuclear factor-kappa beta (NF-κB)/p65, the janus kinase (JAK), signal transduction and activation of transcription (STAT) and the nuclear factor erythroid 2-related factor 2 (Nrf2). UV radiation induces pro-inflammatory genes and causes immunosuppression by depleting the number and activity of the epidermal Langerhans cells. Further, UV radiation remodels the ECM by increasing matrixmetalloproteinases (MMP) and reducing structural collagen and elastin. The photoprotective strategies to prevent/treat photoaging and photocarcinogenesis include oral or topical agents that act as sunscreens or counteract the effects of UV radiation on DNA, cellular antioxidant balance, signal transduction pathways, immunology and the ECM. Many of these agents are phytochemical derivatives and include polyphenols and non-polyphenols. The flavonoids are polyphenols and include catechins, isoflavones, proanthocyanidins, and anthocyanins, whereas the non-flavonoids comprise mono phenolic acids and stilbenes. The natural sources of polyphenols include tea, cocoa, grape/wine, soy, pomegranate, and Polypodium leucotomos. The non-phenolic phytochemicals include carotenoids, caffeine and sulphoraphance (SFN). In addition, there are other phytochemical derivatives or whole extracts such as baicalin, flavangenol, raspberry extract, and Photomorphe umbellata with photoprotective activity against UVB radiation, and thereby carcinogenesis.

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Author and article information

Contributors

Ya-Han Huang: hedy9088723@hotmail.com

Po-Yuan Wu: wu.poyuan@gmail.com

Kuo-Ching Wen: kcwen0520@mail.cmu.edu.tw

Chien-Yih Lin: yihlin@asia.edu.tw

Hsiu-Mei Chiang: +886-4-22053366 , hmchiang@mail.cmu.edu.tw

Journal

Journal ID (nlm-ta): BMC Complement Altern Med

Journal ID (iso-abbrev): BMC Complement Altern Med

Title: BMC Complementary and Alternative Medicine

Publisher: BioMed Central (London )

ISSN (Electronic): 1472-6882

Publication date (Electronic): 1 October 2018

Publication date PMC-release: 1 October 2018

Publication date Collection: 2018

Volume: 18

Electronic Location Identifier: 266

Affiliations

[1 ]ISNI 0000 0001 0083 6092, GRID grid.254145.3, Department of Cosmeceutics, , China Medical University, ; 91 Hsueh-Shih Road, Taichung, 40402 Taiwan

[2 ]ISNI 0000 0004 0572 9415, GRID grid.411508.9, Department of Dermatology, , China Medical University Hospital, ; Taichung, 40402 Taiwan

[3 ]ISNI 0000 0001 0083 6092, GRID grid.254145.3, School of Medicine, , China Medical University, ; 91 Hsueh-Shih Road, Taichung, 40402 Taiwan

[4 ]ISNI 0000 0000 9263 9645, GRID grid.252470.6, Department of Biotechnology, , Asia University, ; 500 Liufeng Road, Wufeng District, Taichung City, 41354 Taiwan

Article

Publisher ID: 2308

DOI: 10.1186/s12906-018-2308-4

PMC ID: 6167875

PubMed ID: 30285714

SO-VID: 17a210c5-2f9f-4dd9-b5f7-12e4464b91e1

License:

Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

History

Date received : 27 April 2018

Date accepted : 20 August 2018

Funding

Funded by: China Medical University (TW)

Award ID: CMU103-ASIA-11

Award Recipient : Hsiu-Mei Chiang

Funded by: China Medical University (TW)

Award ID: CMU105-ASIA-08

Award Recipient : Hsiu-Mei Chiang

Funded by: the Ministry of Science and Technology (TW)

Award ID: MOST 104-2320-B-039-006

Award Recipient : Hsiu-Mei Chiang

Custom metadata

ScienceOpen disciplines: Complementary & Alternative medicine

Keywords: oxidative stress,reactive oxygen species,aging,hemeoxygenase-1 (ho-1),extracellular matrix

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ScienceOpen disciplines: Complementary & Alternative medicine

Keywords: oxidative stress, reactive oxygen species, aging, hemeoxygenase-1 (ho-1), extracellular matrix

Protective effects and mechanisms of Terminalia catappa L. methenolic extract on hydrogen-peroxide-induced oxidative stress in human skin fibroblasts

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Abstract

Background

Methods

Results

Conclusions

Electronic supplementary material

Related collections

Stress signalling in stem cells

Most cited references 31

Prevention of cytotoxicity and inhibition of intercellular communication by antioxidant catechins isolated from Chinese green tea.

Pathophysiology of premature skin aging induced by ultraviolet light.

Mechanisms of Photoaging and Cutaneous Photocarcinogenesis, and Photoprotective Strategies with Phytochemicals

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