scholarly journals Antiphotoaging Effects of 3,5-Dicaffeoyl-epi-quinic Acid via Inhibition of Matrix Metalloproteinases in UVB-Irradiated Human Keratinocytes

2020 ◽  
Vol 2020 ◽  
pp. 1-10 ◽  
Author(s):  
Jung Hwan Oh ◽  
Jung Im Lee ◽  
Fatih Karadeniz ◽  
So Young Park ◽  
Youngwan Seo ◽  
...  
Keyword(s):  
Matrix Metalloproteinases ◽  
Quinic Acid ◽  
Human Keratinocytes ◽  
Skin Aging ◽  
Collagen Degradation ◽  
Premature Aging ◽  
Type I ◽  
Dependent Manner ◽  
Protective Effects ◽  
Uvb Irradiation

UVB exposure is one of the causes of several skin complications including but not limited to premature aging, wrinkle formation, and hyperpigmentation. UV-induced skin aging is called photoaging, and oxidative stress-induced overexpression of matrix metalloproteinases (MMPs) is the main reason behind the photoaging-mediated collagen degradation. Natural origin inhibitors of MMPs are regarded as a promising approach to prevent or treat photoaging. Therefore, the present study investigated the protective effects of 3,5-dicaffeoyl-epi-quinic acid (DCEQA) in human HaCaT keratinocytes against UVB irradiation-related dysregulation of MMPs. Changes in the mRNA and protein expression and release of MMP-1, -2, and -9 were observed after UVB irradiation with or without DCEQA treatment. In addition, the effect of DCEQA on the activation of p38, JNK, and ERK MAPKs was analyzed. Treatment of UVB-irradiated HaCaT cells with 10 μM DCEQA significantly suppressed the overexpression of both mRNA and protein of MMP-1, -2, and -9 while slightly increasing the diminished type I procollagen production. UVB-induced activation of MAPKs was also ameliorated by DCEQA treatment in a dose-dependent manner. Results indicated that DCEQA treatment was able to protect keratinocytes from UVB-induced photoaging by inhibiting the stimulated production of MMPs and the related decrease in collagen production. It was suggested that DCEQA downregulated the collagen degradation via inhibition of MAPK activation, which resulted in decreased MMP activity.

scholarly journals The Antiaging Activity of Ergothioneine in UVA-Irradiated Human Dermal Fibroblasts via the Inhibition of the AP-1 Pathway and the Activation of Nrf2-Mediated Antioxidant Genes

2020 ◽  
Vol 2020 ◽  
pp. 1-13 ◽  
Author(s):  
You-Cheng Hseu ◽  
Yugandhar Vudhya Gowrisankar ◽  
Xuan-Zao Chen ◽  
Yi-Chen Yang ◽  
Hsin-Ling Yang
Keyword(s):  
Human Skin ◽  
Food Supplement ◽  
Skin Aging ◽  
Dermal Fibroblasts ◽  
Ros Generation ◽  
Human Skin Fibroblast ◽  
Type I ◽  
Dependent Manner ◽  
Protective Effects ◽  
Antioxidant Genes

UVA irradiation induced ROS-mediated photo damage to the human skin leading to coarseness, wrinkling, pigmentation, and cutaneous malignancies. We investigated the dermatoprotective efficacies of submicromolar concentrations of ergothioneine (EGT, 0.125-0.5 μM), which occurs naturally as a sulfur-containing amino acid, in the mechanisms in human skin fibroblast (HSF) cells. UVA-induced AP-1 (c-Fos and c-Jun) translocation was found to be inhibited by EGT treatments with the parallel inhibition of the collagenolytic matrix metalloproteinase- (MMP-) 1 activation and type I procollagen degradation. Moreover, EGT mitigated UVA-induced ROS generation. An increase in the amount of antioxidant genes (HO-1, NQO-1, and γ-GCLC) from EGT and were associated with upregulated Nrf2 expressions in a dose-dependent or time-dependent manner. We confirmed this from Nrf2 translocation and increased nuclear ARE promoter activity that underlie EGT dermatoprotective activities. Also, glutathione (GSH) levels (from γ-GCLC) were significantly increased. Moreover, we showed that mediated by ERK, JNK, and PKC, signaling cascades mediate Nrf2 translocation. We confirmed this phenomenon by the suppressed nuclear Nrf2 activation in cells that were treated with respective inhibitors (PD98059, SP600125, and GF109203X). However, antioxidant protein expressions were impaired in Nrf2 knockdown cells to confirm that ARE/Nrf2 pathways and the inhibition of AP-1 had significant roles in EGT-mediated protective effects. We can conclude that ergothioneine ameliorated UVA-induced skin aging and is a useful food supplement for skin care products.

Zinc Inhibits Collagenolysis by Cathepsin K and Matrix Metalloproteinases in Demineralized Dentin Matrix

2017 ◽  
Vol 51 (6) ◽  
pp. 576-581 ◽  
Author(s):  
Pinar Altinci ◽  
Roda Seseogullari-Dirihan ◽  
Gulsen Can ◽  
David Pashley ◽  
Arzu Tezvergil-Mutluay
Keyword(s):  
Matrix Metalloproteinases ◽  
Mass Loss ◽  
Type I Collagen ◽  
Cathepsin K ◽  
Collagen Degradation ◽  
Type I ◽  
Level Control ◽  
Physiological Level ◽  
Cysteine Cathepsins ◽  
Demineralized Dentin

The enzymatic degradation of dentin organic matrix occurs via both the action of matrix metalloproteinases (MMPs) and cysteine cathepsins (CCs). Zinc can prevent collagen hydrolysis by MMPs. However, its effect on the activity of dentin-bound CCs is not known. The aim of this study was to investigate the effect of zinc on matrix-bound cathepsin K and MMP activity in dentin. Completely demineralized dentin beams were divided into test groups (n = 9) and incubated at 37°C in an incubation media (1 mL) containing ZnCl2 of 0.02 (physiological level, control), 0.2, 0.5, 1, 5, 10, 20, 30, or 40 mM. The dry mass changes of the beams were determined, and incubation media were analyzed for cathepsin K- and MMP-specific collagen degradation end products - CTX (C-terminal cross-linked telopeptide of type I collagen) and ICTP (cross-linked carboxy-terminal telopeptide of type I collagen) - at 1, 3, and 7 days of incubation. The mass loss of the beams decreased when the zinc level in the incubation media was ≥5 mM (p < 0.05). The release of liberated collagen degradation telopeptides decreased in accordance with the decrease in the mass loss rates of the beams. Cathepsin K-induced dentin collagen degradation can be strongly inhibited by zinc. Zinc levels of ≥5 mM can be considered as a reliable threshold for the stabilization of dentin matrices.

scholarly journals Protection against UVB-Induced Photoaging by Nypa fruticans via Inhibition of MAPK/AP-1/MMP-1 Signaling

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Hee-Jeong Choi ◽  
Md Badrul Alam ◽  
Mi-Eun Baek ◽  
Yoon-Gyung Kwon ◽  
Ji-Young Lim ◽  
...  
Keyword(s):  
Radical Scavenging Activity ◽  
Radical Scavenging ◽  
Reactive Oxygen Species Generation ◽  
Skin Aging ◽  
Current Data ◽  
Collagen Degradation ◽  
Ultraviolet B ◽  
Skin Thickness ◽  
Dependent Manner ◽  
Nypa Fruticans

Ultraviolet B (UVB) irradiation is major causative factor in skin aging. The aim of the present study was to investigate the protective effect of a 50% ethanol extract from Nypa fruticans (NF50E) against UVB-induced skin aging. The results indicated that NF50E exerted potent antioxidant activity (IC50 = 17.55 ± 1.63 and 10.78 ± 0.63 μg/mL for DPPH and ABTS-radical scavenging activity, respectively) in a dose-dependent manner. High-performance liquid chromatography revealed that pengxianencin A, protocatechuic acid, catechin, chlorogenic acid, epicatechin, and kaempferol were components of the extract. In addition, the extract exhibited elastase inhibitory activity (IC50 = 17.96 ± 0.39 μg/mL). NF50E protected against UVB-induced HaCaT cell death and strongly suppressed UVB-stimulated cellular reactive oxygen species generation without cellular toxicity. Moreover, topical application of NF50E mitigated UVB-induced photoaging lesions including skin erythema and skin thickness in BALB/C mice. NF50E treatment inhibited UVB-induced collagen degradation as well as MMP-1 and IL-1β expressions and significantly stimulated SIRT1 expression. Furthermore, the extract treatment markedly suppressed the activation of NF-κB and AP-1 (p-c-Jun) by deactivating the p38 and JNK proteins. Taken together, current data suggest that NF50E exhibits potent antioxidant potential and protection against photoaging by attenuating MMP-1 activity and collagen degradation possibly through the downregulation of MAPK/NF-κB/AP-1 signaling and SIRT1 activation.

scholarly journals Activation of matrix metalloproteinases and FoxO3a in HaCaT keratinocytes by radiofrequency electromagnetic field exposure

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ju Hwan Kim ◽  
Dong-Jun Kang ◽  
Jun-Sang Bae ◽  
Jai Hyuen Lee ◽  
Sangbong Jeon ◽  
...  
Keyword(s):  
Electromagnetic Field ◽  
Matrix Metalloproteinases ◽  
Human Keratinocytes ◽  
Skin Aging ◽  
Ros Generation ◽  
Related Factors ◽  
Apoptotic Pathway ◽  
Field Exposure ◽  
Cell Growth And Viability ◽  
Radiofrequency Electromagnetic Field

AbstractAs the skin is the largest body organ and critically serves as a barrier, it is frequently exposed and could be physiologically affected by radiofrequency electromagnetic field (RF-EMF) exposure. In this study, we found that 1760 MHz RF-EMF (4.0 W/kg specific absorption rate for 2 h/day during 4 days) exposure could induce intracellular reactive oxygen species (ROS) production in HaCaT human keratinocytes using 2′,7′-dichlorofluorescin diacetate fluorescent probe analysis. However, cell growth and viability were unaffected by RF-EMF exposure. Since oxidative stress in the skin greatly influences the skin-aging process, we analyzed the skin senescence-related factors activated by ROS generation. Matrix metalloproteinases 1, 3, and 7 (MMP1, MMP3, and MMP7), the main skin wrinkle-related proteins, were significantly increased in HaCaT cells after RF-EMF exposure. Additionally, the gelatinolytic activities of secreted MMP2 and MMP9 were also increased by RF-EMF exposure. FoxO3a (Ser318/321) and ERK1/2 (Thr 202/Tyr 204) phosphorylation levels were significantly increased by RF-EMF exposure. However, Bcl2 and Bax expression levels were not significantly changed, indicating that the apoptotic pathway was not activated in keratinocytes following RF-EMF exposure. In summary, our findings show that exposure to 1760 MHz RF-EMF induces ROS generation, leading to MMP activation and FoxO3a and ERK1/2 phosphorylation. These data suggest that RF-EMF exposure induces cellular senescence of skin cells through ROS induction in HaCaT human keratinocytes.

scholarly journals PINK1 Mediates the Protective Effects of Thyroid Hormone T3 in Hyperoxia-induced Lung Injury

2021 ◽  
Author(s):  
Yi Zhang ◽  
Guoying Yu ◽  
Naftali Kaminski ◽  
Patty Lee
Keyword(s):  
Thyroid Hormone ◽  
Lung Injury ◽  
Critical Role ◽  
Protective Role ◽  
Type I ◽  
Dependent Manner ◽  
Protective Effects ◽  
Cell Counts ◽  
Hyperoxia Exposure ◽  
Cellular Bioenergetics

Introduction: Hyperoxia can lead to respiratory failure and death. Our previous work demonstrates that oxidant and mitochondrial injury plays a critical role in hyperoxia-induced acute lung injury (HALI). Recently, thyroid hormone has been demonstrated to promote mitochondrial survival in other models of lung injury, but its role in hyperoxia is unknown. Methods: Adult WT mice were pretreated with nebulized triiodothyronine (T3, 40 μg/kg) for 1 or 3 days, or with propylthiouracil (PTU, 100 μg/kg), for 3 days. Following pretreatment, WT mice underwent 72 hours of hyperoxia exposure. WT and PINK1-/- mice were pretreated with nebulized T3 (40 μg/kg) for 3 days or no pretreatment prior to 72h continuous hyperoxia exposure. Bronchoalveolar lavage (BAL), histological changes in cellular composition, and type I cytokine induction were assessed. Lung lysates for mitochondrial cellular bioenergetics markers were analyzed by Western blot. Results: Hyperoxia caused a significant increase in BAL total cell counts and lung cellular infiltrates. Administration of PTU enhanced HALI, while T3 attenuated HALI, inflammation, and oxidants in WT mice. T3 pretreatment increased mitochondrial biogenesis/fusion/mitophagy and decreased ER stress and apoptosis. PINK1-/- mice were more susceptible to hyperoxia than WT mice. Notably, pretreatment with T3 did not attenuate HALI in PINK1-/- mice. T3 pretreatment also increased mitochondrial anti-ROS potential, improved mitochondrial bioenergetics and mitophagy, and attenuated mitochondria-regulated apoptosis, all in a PINK1-dependent manner. Conclusions: Our results highlight a novel protective role for PINK1 in mediating the cytoprotective effects of thyroid hormone in HALI. Therefore, thyroid hormone may represent a potential therapy for ALI.

Salivary type I collagen degradation end-products and related matrix metalloproteinases in periodontitis

2012 ◽  
Vol 40 (1) ◽  
pp. 18-25 ◽  
Author(s):  
Ulvi K. Gursoy ◽  
Eija Könönen ◽  
Sisko Huumonen ◽  
Taina Tervahartiala ◽  
Pirkko J. Pussinen ◽  
...  
Keyword(s):  
Matrix Metalloproteinases ◽  
Type I Collagen ◽  
Collagen Degradation ◽  
Type I ◽  
End Products

scholarly journals A virus hosted in malaria-infected blood protects against T cell-mediated inflammatory diseases by impairing DC function in a type I IFN-dependent manner

2019 ◽  
Author(s):  
Ali Hassan ◽  
Myriam F. Wlodarczyk ◽  
Mehdi Benamar ◽  
Emilie Bassot ◽  
Anna Salvioni ◽  
...  
Keyword(s):  
T Cell ◽  
Inflammatory Diseases ◽  
Rna Virus ◽  
Host Immune System ◽  
Type I ◽  
Dependent Manner ◽  
Protective Effects ◽  
Type I Ifn ◽  
Experimental Cerebral Malaria ◽  
Beneficial Effects

AbstractCo-infections shape the host immune status, thereby influencing the development of inflammatory diseases, which can result in detrimental or beneficial effects. For example, co-infections with concurrent Plasmodium species can alter malaria clinical evolution and malaria infection itself has the ability to modulate autoimmune reactions but, in both cases, the underlying mechanisms remain ill-defined.Here, we demonstrate that the protective effects of certain rodent malaria strains on T cell-mediated inflammatory pathologies are due to an RNA virus co-hosted in malaria-parasitized blood. We show that live as well as extracts of blood parasitized by P. berghei K173 or P. yoelii 17X YM, confer full protection against Pb ANKA (PbA)-induced Experimental Cerebral Malaria (ECM) and MOG/CFA-induced experimental autoimmune encephalomyelitis (EAE), and that this is associated with a strong type I IFN signature. We detected the presence of a viral element, the RNA virus Lactate Dehydrogenase-elevating Virus (LDV), in the protective Plasmodium stabilates and we established that infection with LDV alone recapitulates the protective effects on ECM and EAE. In ECM, we further show that protection results from an IFN-I-mediated reduction in the abundance of splenic conventional dendritic cell and in their ability to produce the Th1-inducing IL-12p70, leading to a decrease in pathogenic CD4+ Th1 responses. In EAE, protection is achieved by IFN-I mediated blunting of IL-12 and IL-23, preventing the differentiation of IFN-γ-, IL-17- and GM-CSF-producing encephalitogenic CD4+ T cells.Thus, our results identify a virus that is co-hosted in several Plasmodium stabilates across the community and has major consequences on the host immune system. Moreover, our data emphasize the importance of considering concurrent infections for the understanding of autoimmunity and malaria-associated inflammatory complications.

Skin Specific Cells and UVB Damage An experimental assessment

2017 ◽  
Vol 68 (6) ◽  
pp. 1229-1233
Author(s):  
Ioana Zinuca Pavel ◽  
Oana Andrada Iftode ◽  
Iulia Pinzaru ◽  
Dorina Coricovac ◽  
Alina Moaca ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Human Keratinocytes ◽  
Cellular Transformation ◽  
Dependent Manner ◽  
Protective Effects ◽  
Post Exposure ◽  
Skin Cancers ◽  
Ultraviolet Radiation Exposure ◽  
Normal Human ◽  
Uvb Exposure

The alarming increased incidence of skin cancers is closely related to ultraviolet radiation exposure, known to induce cellular transformation in epidermal and dermal layers. The current study describes the behavior of normal (human keratinocytes � HaCat and fibroblasts -1BR3) and tumor cells (human � A375 and murine � B164A5 and B16-F0 - melanoma) after UVB irradiation. A dose of 40 mJ/cm2 (312 nm) led to a decrease of both normal and tumor cells viability in a post-exposure time dependent manner, the most statistically significant reduction being recorded at 24h post-exposure. Moreover, some changes in the shape of cells exposed to UVB were detected. Our results confirm the cytotoxic effects associated with UVB exposure and could be further employed to evaluate the photo-protective effects of different agents.

scholarly journals Conditioned Medium from Human Adipose-Derived Mesenchymal Stem Cell Culture Prevents UVB-Induced Skin Aging in Human Keratinocytes and Dermal Fibroblasts

2019 ◽  
Vol 21 (1) ◽  
pp. 49 ◽  
Author(s):  
Lu Li ◽  
Hien T.T. Ngo ◽  
Eunson Hwang ◽  
Xuan Wei ◽  
Ying Liu ◽  
...  
Keyword(s):  
Conditioned Medium ◽  
Transforming Growth Factor ◽  
Human Keratinocytes ◽  
Transforming Growth Factor Β ◽  
Antioxidant Response ◽  
Skin Aging ◽  
Dermal Fibroblasts ◽  
Heme Oxygenase 1 ◽  
Type I ◽  
Matrix Metalloproteinase 1

Human adipose-derived mesenchymal stem cells-conditioned medium (ADSC-CM) contains cytokines and growth factors that can facilitate the regeneration and repair of various tissues and organs. In the present study, the protective activity of ADSC-CM treatment was investigated in UVB-irradiated human keratinocyte cell line HaCaTs and normal human dermal fibroblasts (NHDFs). It was found that ADSC-CM can modulate the expression of the signaling molecules in the early UVB responsive signaling pathways, including mitogen activated protein kinases (MAPKs), activator protein 1 (AP-1), and nuclear factor kappa B (NF-κB). In addition, ADSC-CM treatment could upregulate antioxidant response element (ARE) such as phase II gene heme oxygenase-1 (HO-1) and increase the expression of collagen synthesis enhancer gene transforming growth factor-β (TGF-β). The expression of matrix metalloproteinase-1 (MMP-1) and procollagen type I synthesis inhibitors such as interleukin-6 (IL-6) was also found to be suppressed upon ADSC-CM treatment. Taken together, our study illustrates the anti-photoaging activities of ADSC-CM in cell-based models.

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