Prevention of the Ultraviolet B-Mediated Skin Photoaging by a Nuclear Factor κB Inhibitor, Parthenolide

Tanaka, Kiyotaka; Hasegawa, Junichi; Asamitsu, Kaori; Okamoto, Takashi

doi:10.1124/jpet.105.088674

Cited by 93 publications

(60 citation statements)

References 42 publications

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“…Acute exposure to UVB triggers NF-κB system in keratinocytes and skin fibroblasts. NF-κB inhibitors can suppress the changes evoked by UV light in skin, which supports the role of NF-κB system in the photoaging process [36].…”

Section: Nf-κb Pathway: Sensor Of Stress and Immune Insultssupporting

confidence: 58%

NF-κB Signaling in the Aging Process

2009

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Introduction The aging process represents a progressive decline in cellular and organism function. Explaining the aging process has given rise to a cornucopia for different theories in which the basic difference has been the question whether aging is genetically regulated or an entropic degeneration process. Discussion Different screening techniques have revealed that mammalian aging is associated with the activation of NF-κB transcription factor system. The NF-κB system is an ancient host defense system concerned with immune responses and different external and internal dangers, such as oxidative and genotoxic stress. NF-κB signaling is not only the master regulator of inflammatory responses but can also regulate several homeostatic responses such as apoptosis, autophagy, and tissue atrophy. We will describe how chronic activation of NF-κB signaling has the capacity to induce the senescent phenotype associated with aging.

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Section: Nf-κb Pathway: Sensor Of Stress and Immune Insultssupporting

confidence: 58%

NF-κB Signaling in the Aging Process

2009

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“…(Saliou et al, 1999;Kim et al, 2001;Wenk et al, 2004). In previous study, it is also reported that UVB-mediated skin photoaging is prevented by suppression of NF-κB activation (Adhami et al, 2003;Tanaka et al, 2005Tanaka et al, , 2007. Thus, inhibition of the NF-κB activation pathway is important for the UVB-mediated skin damage.…”

Section: Suppressive Effect Of Cordycepin On Uvb-induced Nf-κb Activamentioning

confidence: 85%

Cordycepin inhibits UVB-induced matrix metalloproteinase expression by suppressing the NF--κB pathway in human dermal fibroblasts

et al. 2009

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Cordycepin (3'-deoxyadenosine) has been shown to exhibit many pharmacological activities, including anti-cancer, anti-inflammatory, and anti-infection activities. However, the anti-skin photoaging effects of cordycepin have not yet been reported. In the present study, we investigated the inhibitory effects of cordycepin on matrix metalloproteinase-1 (MMP-1) and -3 expressions of the human dermal fibroblast cells. Western blot analysis and real-time PCR revealed cordycepin inhibited UVB-induced MMP-1 and -3 expressions in a dose-dependent manner. UVB strongly activated NF-κB activity, which was determined by IκBα degradation, nuclear localization of p50 and p65 subunit, and NF-κB binding activity. However, UVB-induced NF-κB activation and MMP expression were completely blocked by cordycepin pretreatment. These findings suggest that cordycepin could prevent UVB-induced MMPs expressions through inhibition of NF-κB activation. In conclusion, cordycepin might be used as a potential agent for the prevention and treatment of skin photoaging.

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“…These cellular processes are related to photoaging and photocarcinogenesis [12,13]. UV-mediated DNA damage is mainly attributed to the formation of cyclobutane pyrimidine dimers (CPDs) between adjacent thymine (T) or cytosine (C) residues, or to a lesser extent, formation of pyrimidine (6-4) pyrimidone photoproducts (6-4PPs) via direct absorption of UV photons by the DNA bases [14,15].…”

Section: Introduction Introduction Introduction Introductionmentioning

confidence: 99%

Effects of UV wavelength on cell damages caused by UV irradiation in PC12 cells

Masuma

Kashima

Kurasaki

et al. 2013

Journal of Photochemistry and Photobiology B: Biology

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Ultraviolet (UV) radiations present in sunlight are a major etiologic factor for many skin diseases and induce DNA damage through formation of cyclobutane pyrimidine dimer (CPD). This study was conducted to determine the toxicological effects of different wavelengths (250, 270, 290, and 310 nm) and doses of UV radiation on cell viability, DNA structure, and DNA damage repair mechanisms in a PC12 cell system. For this, we evaluated cell viability and CPD formation. Cell survival rate was markedly decreased 24 h after UV irradiation in a dose-dependent manner at all wavelengths (except at 310 nm). Cell viability increased with increasing wavelength in the following order: 250 < 270 < 290 < 310 nm. UV radiation at 250 nm showed the highest cell killing ability, with a median lethal dose (LD50) of 120 mJ/cm2. The LD50 gradually increased with increase in wavelength. Among the 4 wavelengths tested, the highest LD50 (6000 mJ/cm2) was obtained for 310 nm. CPD formation decreased substantially with increasing wavelength. Among the 4 wavelengths, the proportion of CPD formation was highest at 250 nm and lowest at 310 nm. On the basis of LD50 values for each wavelength, PC12 cells irradiated with UV radiation of 290 nm showed maximum DNA repair ability, whereas those irradiated with the 310-nm radiation did not show any repair ability. Toxicity of UV radiation varied with wavelengths and exposure doses

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Prevention of the Ultraviolet B-Mediated Skin Photoaging by a Nuclear Factor κB Inhibitor, Parthenolide

Cited by 93 publications

References 42 publications

NF-κB Signaling in the Aging Process

NF-κB Signaling in the Aging Process

Cordycepin inhibits UVB-induced matrix metalloproteinase expression by suppressing the NF--κB pathway in human dermal fibroblasts

Effects of UV wavelength on cell damages caused by UV irradiation in PC12 cells

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