Isorhamnetin Protects Human Keratinocytes against Ultraviolet B-Induced Cell Damage

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Abstract

Isorhamnetin (3-methylquercetin) is a flavonoid derived from the fruits of certain medicinal plants. This study investigated the photoprotective properties of isorhamnetin against cell damage and apoptosis resulting from excessive ultraviolet (UV) B exposure in human HaCaT keratinocytes. Isorhamnetin eliminated UVB-induced intracellular reactive oxygen species (ROS) and attenuated the oxidative modification of DNA, lipids, and proteins in response to UVB radiation. Moreover, isorhamnetin repressed UVB-facilitated programmed cell death in the keratinocytes, as evidenced by a reduction in apoptotic body formation, and nuclear fragmentation. Additionally, isorhamnetin suppressed the ability of UVB light to trigger mitochondrial dysfunction. Taken together, these results indicate that isorhamnetin has the potential to protect human keratinocytes against UVB-induced cell damage and death.

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Toxic effects of ultraviolet radiation on the skin.

Yasuhiro Matsumura, Honnavara Ananthaswamy (2004)

Ultraviolet (UV) irradiation present in sunlight is an environmental human carcinogen. The toxic effects of UV from natural sunlight and therapeutic artificial lamps are a major concern for human health. The major acute effects of UV irradiation on normal human skin comprise sunburn inflammation (erythema), tanning, and local or systemic immunosuppression. At the molecular level, UV irradiation causes DNA damage such as cyclobutane pyrimidine dimers and (6-4) photoproducts, which are usually repaired by nucleotide excision repair (NER). Chronic exposure to UV irradiation leads to photoaging, immunosuppression, and ultimately photocarcinogenesis. Photocarcinogenesis involves the accumulation of genetic changes, as well as immune system modulation, and ultimately leads to the development of skin cancers. In the clinic, artificial lamps emitting UVB (280-320 nm) and UVA (320-400 nm) radiation in combination with chemical drugs are used in the therapy of many skin diseases including psoriasis and vitiligo. Although such therapy is beneficial, it is accompanied with undesirable side effects. Thus, UV radiation is like two sides of the same coin--on one side, it has detrimental effects, and on the other side, it has beneficial effects.

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Protein carbonyl groups as biomarkers of oxidative stress.

Isabella Dalle-Donne, Aldo Milzani, Daniela Giustarini … (2003)

Oxidative stress, an imbalance toward the pro-oxidant side of the pro-oxidant/antioxidant homeostasis, occurs in several human diseases. Among these diseases are those in which high levels of protein carbonyl (CO) groups have been observed, including Alzheimer's disease (AD), rheumatoid arthritis, diabetes, sepsis, chronic renal failure, and respiratory distress syndrome. What relationships might be among high level of protein CO groups, oxidative stress, and diseases remain uncertain.The usage of protein CO groups as biomarkers of oxidative stress has some advantages in comparison with the measurement of other oxidation products because of the relative early formation and the relative stability of carbonylated proteins. Most of the assays for detection of protein CO groups involve derivatisation of the carbonyl group with 2,4-dinitrophenylhydrazine (DNPH), which leads to formation of a stable dinitrophenyl (DNP) hydrazone product. This then can be detected by various means, such as spectrophotometric assay, enzyme-linked immunosorbent assay (ELISA), and one-dimensional or two-dimensional electrophoresis followed by Western blot immunoassay. At present, the measurement of protein CO groups after their derivatisation with DNPH is the most widely utilized measure of protein oxidation.

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Ultraviolet light and osmotic stress: activation of the JNK cascade through multiple growth factor and cytokine receptors.

C Rosette, M Karin (1996)

Exposure of mammalian cells to ultraviolet (UV) light or high osmolarity strongly activates the c-Jun amino-terminal protein kinase (JNK) cascade, causing induction of many target genes. Exposure to UV light or osmotic shock induced clustering and internalization of cell surface receptors for epidermal growth factor (EGF), tumor necrosis factor (TNF), and interleukin-1 (IL-1). Activation of the EGF and TNF receptors was also detected biochemically. Whereas activation of each receptor alone resulted in modest activation of JNK, coadministration of EGF, IL-1, and TNF resulted in a strong synergistic response equal to that caused by exposure to osmotic shock or UV light. Inhibition of clustering or receptor down-regulation attenuated both the osmotic shock and UV responses. Physical stresses may perturb the cell surface or alter receptor conformation, thereby subverting signaling pathways normally used by growth factors and cytokines.

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Author and article information

Journal

Journal ID (nlm-ta): Biomol Ther (Seoul)

Journal ID (iso-abbrev): Biomol Ther (Seoul)

Journal ID (publisher-id): Biomol Ther (Seoul)

Journal ID (publisher-id): ksp

Title: Biomolecules & Therapeutics

Publisher: The Korean Society of Applied Pharmacology

ISSN (Print): 1976-9148

ISSN (Electronic): 2005-4483

Publication date (Print): July 2015

Publication date (Electronic): 01 July 2015

Volume: 23

Issue: 4

Pages: 357-366

Affiliations

[1 ]School of Medicine, Jeju National University, Jeju 690-756

[2 ]Department of Mechanical Engineering & Graduate School of Medical Science and Engineering, KAIST, Daejeon 305-701

[3 ]National Fusion Research Institute, Plasma Technology Research Center, Gunsan 573-540

[4 ]Aging Research Center, Korea Institute of Oriental Medicine, Daejeon 305-811, Republic of Korea

Author notes

[* ]Corresponding Author: E-mail: jinwonh@ 123456jejunu.ac.kr , Tel: +82-64-754-3838, Fax: +82-64-702-2687

Article

Publisher ID: bt-23-357

DOI: 10.4062/biomolther.2015.005

PMC ID: 4489831

SO-VID: 39ccf242-bcd0-4ba2-a299-d7d008f50d32

License:

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

History

Date received : 09 January 2015

Date revision received : 29 January 2015

Date accepted : 26 February 2015

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Isorhamnetin Protects Human Keratinocytes against Ultraviolet B-Induced Cell Damage

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Cancer Immunotherapy

Most cited references 35

Toxic effects of ultraviolet radiation on the skin.

Protein carbonyl groups as biomarkers of oxidative stress.

Ultraviolet light and osmotic stress: activation of the JNK cascade through multiple growth factor and cytokine receptors.

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