23‐Hydroxytormentic acid protects human dermal fibroblasts by attenuating <scp>UVA</scp>‐induced oxidative stress

Youn, Hae Jeong; Kim, Ki Bbeum; Han, Hyo-Sun; An, In‐Sook; Ahn, Kyu Joong

doi:10.1111/phpp.12294

Cited by 9 publications

(9 citation statements)

References 24 publications

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“…Therefore, the inhibition of ROS production and lysosome contents was due to the ability of ES-GNPs to reduce HDF senescence by stimulating UVA irradiation. Senescence related proteins including p16, p21 and p-p53 have also been proposed to play a critical role in UVA-irradiated HDF senescence [4]. In our study, we found that treatment with ES-GNPs inhibited the expression level of p16, p21 and p-p53, indicating the dependence of p16, p21 and p-p53 in ES-GNP-initiated anticellular senescence effects.…”

Section: Discussionsupporting

confidence: 58%

“…A hypothetical hydrolase, e.g., SA-β-galactosidase, is commonly used as an indirect essential maker of senescent cells. There is evidence showing that the HDF senescence caused by UVA irradiation could cause the increase of SA-β-galactosidase activity [4]. In our study, UVA irradiation caused an increase in SA-β-galactosidase activity in HDF, while intervention with ES-GNPs noticeably diminished the impact thereof.…”

Section: Discussionsupporting

confidence: 44%

“…Taken together, these changes in UVA irradiated HDFs contribute to the initiation and progression of skin-photoaging. UVA irradiated HDFs exhibit upregulation of MMP-1/-3, which then upregulate cellular senescence in UVA-irradiated HDFs [4]. To further investigate the mechanisms of the antisenescence effect of ES-GNPs via MMP-1/-3, we studied the effects of the ES-GNPs on the transcription and translation of MMP-1/-3 in the UVA-irradiated group.…”

Section: Es-gnps Downregulate Mmp−1/−3 Mrna Protein Expression and Smentioning

confidence: 99%

“…UVA irradiation can penetrate the epidermal and dermal layers of the skin, and contribute to oxidative stress, premature skin aging, and photo-carcinogenesis. Sustained exposure to UVA affects cell growth and survival, and induces DNA damage, the production of reactive oxygen species (ROS), and senescence-associated β-galactosidase (SA-β-galactosidase) activity [3,4]. Repeated exposure of human dermal fibroblasts (HDFs) to UVA irradiation has been established as a cellular senescence model to investigate certain characteristics of epidermal and dermal skin photoaging.…”

Section: Introductionmentioning

confidence: 99%

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Gold Nanoparticles Using Ecklonia stolonifera Protect Human Dermal Fibroblasts from UVA-Induced Senescence through Inhibiting MMP-1 and MMP-3

Jun

Kim

et al. 2020

Marine Drugs

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The effect of gold nanoparticles (GNPs) synthesized in marine algae has been described in the context of skin, where they have shown potential benefit. Ecklonia stolonifera (ES) is a brown algae that belongs to the Laminariaceae family, and is widely used as a component of food and medicine due to its biological activities. However, the role of GNPs underlying cellular senescence in the protection of Ecklonia stolonifera gold nanoparticles (ES-GNPs) against UVA irradiation is less well known. Here, we investigate the antisenescence effect of ES-GNPs and the underlying mechanism in UVA-irradiated human dermal fibroblasts (HDFs). The DPPH and ABTS radical scavenging activity of ES extracts was analyzed. These analyses showed that ES extract has potent antioxidant properties. The facile and optimum synthesis of ES-GNPs was established using UV-vis spectra. The surface morphology and crystallinity of ES-GNPs were demonstrated using high resolution transmission electron microscopy (HR-TEM), energy dispersive spectroscopy (EDS), X-ray diffraction (XRD), and Fourier-transform infrared spectroscopy (FT-IR). ES-GNPs presented excellent photocatalytic activity, as shown by the photo-degradation of methylene blue and rhodamine B. A cellular senescence model was established by irradiating HDFs with UVA. UVA-irradiated HDFs exhibited increased expression of senescence-associated β-galactosidase (SA-β-galactosidase). However, pretreatment with ES-GNPs resulted in reduced SA-β-galactosidase activity in UVA-irradiated HDFs. Intracellular ROS levels and G1 arrest in UVA-irradiated HDFs were checked against the background of ES-GNP treatment to investigate the antisenescence effects of ES-GNPs. The results showed that ES-GNPs significantly inhibit UVA-induced ROS levels and G1 arrest. Importantly, ES-GNPs significantly downregulated the transcription and translation of MMP (matrix metalloproteinases)-1/-3, which regulate cellular senescence in UVA-irradiated HDFs. These findings indicate that our optimal ES-GNPs exerted an antisenescence effect on UVA-irradiated HDFs by inhibiting MMP-1/-3 expression. Collectively, we posit that ES-GNPs may potentially be used to treat photoaging of the skin.

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Section: Discussionsupporting

confidence: 58%

Section: Discussionsupporting

confidence: 44%

Section: Es-gnps Downregulate Mmp−1/−3 Mrna Protein Expression and Smentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Gold Nanoparticles Using Ecklonia stolonifera Protect Human Dermal Fibroblasts from UVA-Induced Senescence through Inhibiting MMP-1 and MMP-3

Jun

Kim

et al. 2020

Marine Drugs

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“…Long-term UVR irradiation causes skin damage, leading to skin photoaging, and the main damage is in the dermis, which is also the main area for repairing skin trauma [18]. UVA can penetrate the dermal layer of the skin [19]. So, it is worth mentioning that UVA mainly influences the human papillary dermis fibroblasts.…”

Section: Discussionmentioning

confidence: 99%

Concentrated Growth Factors Can Inhibit Photoaging Damage Induced by Ultraviolet A (UVA) on the Human Dermal Fibroblasts In Vitro

et al. 2019

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Background Photoaging is the main cause of extrinsic skin aging. Daily exposure to ultraviolet A (UVA) accelerates the process of photoaging. The present study aimed to understand the role of concentrated growth factors (CGF) on UVA irradiated human skin cells. Material/Methods We isolated and subcultured normal human dermal fibroblasts (NHDFs) from 6 different human dorsal skins and established photoaging models of NHDFs irradiated by UVA to detect the influence of CGF on fibroblasts in vitro . Three groups were examined: normal, cellular photoaging model (total dosages of 18J·cm −2 ), and cellular photoaging model plus CGF. In our study, we used the MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide) assay method to measure the cell viability. We also used reactive oxygen species (ROS) assay and superoxide dismutase (SOD) assay to measure respectively the amount of oxygen free radicals and antioxidative enzymes. We compared the migration rates among the photoaging model groups, the control groups, and the CGF-treated culture medium groups that were irradiated. Results Our study results indicated that 5% CGF can reduce UVA-induced human skin fibroblasts damage significantly, improve the viability of NHDFs significantly, and largely decrease the UVA irradiation effect ( P <0.05). The migration rates of the normal group and the UVA-irradiated NHDFs in the 5% CGF group had significantly increased migration rates ( P <0.05), compared to the control medium group. The migration rates of the UVA-irradiated NHDFs in 5% CGF exceed those of the normal group. These results showed that 5% CGF could greatly promote cellular proliferation, migration, and SOD at the same time that the amounts of ROS were markedly decreased. Conclusions These experimental findings offer some important insights into CGF’s capacity for scavenging ROS, improving SOD, and increasing migration rates in NHDFs irradiated by UVA.

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23-Hydroxytormentic acid reduces cerebral ischemia/reperfusion damage in rats through anti-apoptotic, antioxidant, and anti-inflammatory mechanisms

Wang

Liu

2021

Naunyn-Schmiedeberg's Arch Pharmacol

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23‐Hydroxytormentic acid protects human dermal fibroblasts by attenuating UVA‐induced oxidative stress

Abstract: In conclusion, 23-HTA protects against and attenuates UVA-induced oxidative stress in NHDFs likely via the nuclear factor erythroid-derived 2-like 2 signaling pathway.

Cited by 9 publications

References 24 publications

Gold Nanoparticles Using Ecklonia stolonifera Protect Human Dermal Fibroblasts from UVA-Induced Senescence through Inhibiting MMP-1 and MMP-3

Gold Nanoparticles Using Ecklonia stolonifera Protect Human Dermal Fibroblasts from UVA-Induced Senescence through Inhibiting MMP-1 and MMP-3

Concentrated Growth Factors Can Inhibit Photoaging Damage Induced by Ultraviolet A (UVA) on the Human Dermal Fibroblasts In Vitro

23-Hydroxytormentic acid reduces cerebral ischemia/reperfusion damage in rats through anti-apoptotic, antioxidant, and anti-inflammatory mechanisms

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