UVB damage onset and progression 24 h post exposure in human-derived skin cells

Khalil, Christian; Shebaby, Wassim N.

doi:10.1016/j.toxrep.2017.07.008

Cited by 43 publications

(32 citation statements)

References 54 publications

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“…The oxidative stress induced by UVB is also involved in the activation of the intrinsic apoptotic signaling pathway [30]. Our data showed that excessive ROS levels, especially H 2 O 2 , associated with a decrease of the endogenous antioxidant system induced by UVB on L929 cells, caused the loss of Δ ψ m, and significantly activated caspase 9, as observed by western blotting assays.…”

Section: Discussionsupporting

confidence: 60%

“…The MAPK signaling pathway is activated by large amounts of ROS produced in cells irradiated with UVB, followed by downstream transcription factor phosphorylation, leading to the expression of apoptotic factors and MMPs [5, 30]. Since DHCA reduces apoptosis and MMP expression, we intended to verify whether DHCA may act by inhibiting phosphorylation of the MAPK subfamilies JNK and p38 (Figure 7(b)).…”

Section: Resultsmentioning

confidence: 99%

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Dihydrocaffeic Acid Prevents UVB-Induced Oxidative Stress Leading to the Inhibition of Apoptosis and MMP-1 Expression via p38 Signaling Pathway

Oliveira

Ratti

Daré

et al. 2019

Oxidative Medicine and Cellular Longevity

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Chronic UVB exposure promotes oxidative stress, directly causes molecular damage, and induces aging-related signal transduction, leading to skin photoaging. Dihydrocaffeic acid (DHCA) is a phenolic compound with potential antioxidant capacity and is thus a promising compound for the prevention of UVB-induced skin photodamage. The aim of this study was to evaluate the antioxidant and protective effect of DHCA against oxidative stress, apoptosis, and matrix metalloproteinase (MMP) expression via the mitogen-activated protein kinase (MAPK) signaling pathway on L929 fibroblasts irradiated with UVB. DHCA exhibited high antioxidant capacity on 2,2-diphenyl-1-picrylhydrazyl (DPPH•), 2,2-azinobis-3-ethylbenzothiazoline-6-sulphonic acid (ABTS•+), and xanthine/luminol/xanthine oxidase (XOD) assays and reduced UVB-induced cell death in the neutral red assay. DHCA also modulated oxidative stress by decreasing intracellular reactive oxygen species (ROS) and extracellular hydrogen peroxide (H2O2) production, enhancing catalase (CAT) and superoxide dismutase (SOD) activities and reduced glutathione (GSH) levels. Hence, cellular damage was attenuated by DHCA, including lipid peroxidation, apoptosis/necrosis and its markers (loss of mitochondria membrane potential, DNA condensation, and cleaved caspase 9 expression), and MMP-1 expression. Furthermore, DHCA reduced the phosphorylation of MAPK p38. These findings suggest that DHCA can be used in the development of skin care products to prevent UVB-induced skin damage.

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Section: Discussionsupporting

confidence: 60%

Section: Resultsmentioning

confidence: 99%

Dihydrocaffeic Acid Prevents UVB-Induced Oxidative Stress Leading to the Inhibition of Apoptosis and MMP-1 Expression via p38 Signaling Pathway

Oliveira

Ratti

Daré

et al. 2019

Oxidative Medicine and Cellular Longevity

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“…61 Many signaling pathways are involved, including p53-mediated activation of pro-apoptotic factors as a result of DNA double-stranded breaks, MAP-kinase activation, and the capacity for DNA repair. [62][63][64] It was previously demonstrated that Ru(II) anticancer drugs can trigger DNA damage which in turn activates apoptosis via the intrinsic pathway. 65 Zhang and coworkers reported the intercalative potential of Ru(II) polypyridyl complexes which were shown to induce apoptosis in A549 cells, as concluded from ow cytometric studies.…”

Section: Resultsmentioning

confidence: 99%

Enhanced cellular uptake and photochemotherapeutic potential of a lipophilic strained Ru(ii) polypyridyl complex

et al. 2019

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“…UVA is absorbed by chromophores in dermal cells to induce the generation of ROS that indirectly cause oxidative damage to DNA, leading to mutations and cancer (Farrar et al, 2018;Rybchyn et al, 2018). In contrast, UVB damages the membranes and proteins of cells on the surface layer of skin and superficial layer of the dermis, leading to sunburn erythema that can result in skin cancer in extreme cases (Khalil and Shebaby, 2017;Raad et al, 2017). ROS can activate the expression of MMPs that degrade the extracellular matrix including collagen and elastin fibers in the dermis, which can cause wrinkles, dandruff, and dullness (Burnstock et al, 2012;Ryu et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

Caffeine Targets SIRT3 to Enhance SOD2 Activity in Mitochondria

Gan

Gao

et al. 2020

Front. Cell Dev. Biol.

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Caffeine is chemically stable and not readily oxidized under normal physiological conditions but also has antioxidant effects, although the underlying molecular mechanism is not well understood. Superoxide dismutase (SOD) 2 is a manganesecontaining enzyme located in mitochondria that protects cells against oxidative stress by scavenging reactive oxygen species (ROS). SOD2 activity is inhibited through acetylation under conditions of stress such as exposure to ultraviolet (UV) radiation. Sirtuin 3 (SIRT3) is the major mitochondrial nicotinamide adenine dinucleotide (NAD +)-dependent deacetylase, which deacetylates two critical lysine residues (lysine 68 and lysine 122) on SOD2 and promotes its antioxidative activity. In this study, we investigated whether the antioxidant effect of caffeine involves modulation of SOD2 by SIRT3 using in vitro and in vivo models. The results show that caffeine interacts with SIRT3 and promotes direct binding of SIRT3 with its substrate, thereby enhancing its enzymatic activity. Mechanistically, caffeine bound to SIRT3 with high affinity (K D = 6.858 × 10 −7 M); the binding affinity between SIRT3 and its substrate acetylated p53 was also 9.03 (without NAD +) or 6.87 (with NAD +) times higher in the presence of caffeine. Caffeine effectively protected skin cells from UV irradiation-induced oxidative stress. More importantly, caffeine enhanced SIRT3 activity and reduced SOD2 acetylation, thereby leading to increased SOD2 activity, which could be reversed by treatment with the SIRT3 inhibitor 3-(1H-1,2,3-triazol-4-yl) pyridine (3-TYP) in vitro and in vivo. Taken together, our results show that caffeine targets SIRT3 to enhance SOD2 activity and protect skin cells from UV irradiation-induced oxidative stress. Thus, caffeine, as a small-molecule SIRT3 activator, could be a potential agent to protect human skin against UV radiation.

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UVB damage onset and progression 24 h post exposure in human-derived skin cells

Abstract: Graphical abstract

Cited by 43 publications

References 54 publications

Dihydrocaffeic Acid Prevents UVB-Induced Oxidative Stress Leading to the Inhibition of Apoptosis and MMP-1 Expression via p38 Signaling Pathway

Dihydrocaffeic Acid Prevents UVB-Induced Oxidative Stress Leading to the Inhibition of Apoptosis and MMP-1 Expression via p38 Signaling Pathway

Enhanced cellular uptake and photochemotherapeutic potential of a lipophilic strained Ru(ii) polypyridyl complex

Caffeine Targets SIRT3 to Enhance SOD2 Activity in Mitochondria

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