scholarly journals Chronic Ultraviolet Irradiation to the Skin Dysregulates Adrenal Medulla and Dopamine Metabolism In Vivo

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 920
Author(s):  
Hye-Sun Lim ◽  
Kyeong-No Yoon ◽  
Jin Ho Chung ◽  
Yong-Seok Lee ◽  
Dong Hun Lee ◽  
...  
Keyword(s):  
Adrenal Glands ◽  
Mouse Skin ◽  
Dopamine Metabolism ◽  
The Body ◽  
Catecholamine Metabolism ◽  
Uvb Radiation ◽  
Defense Proteins ◽  
Uvb Irradiation ◽  
Uvb Exposure

Ultraviolet (UV) radiation has a strong biological effect on skin biology, and it switches on adaptive mechanisms to maintain homeostasis in organs such as the skin, adrenal glands, and brain. In this study, we examined the adaptation of the body to repeated bouts of UVB radiation, especially with respect to the catecholamine synthesis pathway of the adrenal glands. The effects of UVB on catecholamine-related enzymes were determined by neurochemical and histological analyses. To evaluate catecholamine changes after chronic excessive UVB irradiation of mouse skin, we examined dopamine and norepinephrine levels in the adrenal glands and blood from UV-irradiated and sham-irradiated mice. We found that chronic excessive UVB exposure significantly reduced dopamine levels in both tissues but did not affect norepinephrine levels. In addition, UVB irradiation significantly increased the levels of related enzymes tyrosine hydroxylase and dopamine-β-hydroxylase. Furthermore, we also found that apoptosis-associated markers were increased and that oxidative defense proteins were decreased, which might have contributed to the marked structural abnormalities in the adrenal medullas of the chronically UVB-irradiated mice. This is the first evidence of the damage to the adrenal gland and subsequent dysregulation of catecholamine metabolism induced by chronic exposure to UVB.

scholarly journals Almond Consumption Increased UVB Resistance in Healthy Asian Women

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 319-319
Author(s):  
Susanne Henning ◽  
Jason Li ◽  
Gail Thames ◽  
Omar Bari ◽  
Patrick Tran ◽  
...  
Keyword(s):  
Skin Aging ◽  
Ultraviolet B ◽  
In Vivo Studies ◽  
Asian Women ◽  
Skin Extract ◽  
Uvb Radiation ◽  
Facial Skin ◽  
Uvb Exposure

Abstract Objectives Almonds are a rich source of phenolic and polyphenolic compounds, which have antioxidant activity. In vitro and in vivo studies have demonstrated that topical application of almond oil and almond skin extract reduces UVB-induced photoaging. Ultraviolet-B (UVB) protection by oral almond consumption has not been previously studied in humans. It was the objective to investigate whether oral almond consumption can increase resistance to UVB radiation and reduce skin aging in healthy Asian women. Methods Thirty-nine female participants (18–45 years) with Fitzpatrick skin type II-IV were randomly assigned to consume either 1.5 oz of almonds or 1.8 oz of pretzels daily for 12 weeks. Minimal erythema dose (MED) was determined using a standardized protocol, which determined the minimal radiation inducing erythema on the inner arm 24 hours following UVB exposure. Facial skin texture was evaluated by two dermatologists using the Clinician's Erythema Assessment scale and Allergan Roughness scale. Facial melanin index, hydration, sebum, and erythema were determined using a cutometer. Results Women who consumed almonds, experienced a significant increase in MED from 415 ± 64 to 487 ± 59 (18.7 ± 19.2%, P = 0.006) from baseline to week 12 compared to women in the pretzel group from 415 ± 67 to 421 ± 67 (1.8 ± 11.1%). The exposure time to reach minimal erythema was also increased significantly in the almond group from 160 ± 23 to 187 ± 25 (17.5 ± 22.2%) compared to the pretzel group from 165 ± 27 to 166 ± 25 (1.7 ± 14%) (p=0.026). There were no differences noted between the groups consuming almonds versus pretzels in Allergan roughness, melanin, hydration, or sebum on facial skin. Conclusions Our findings suggest that daily oral almond consumption may lead to enhanced protection from UVB photodamage by increasing the MED. Protection from other UV radiation was not tested and therefore almond consumption will not replace other methods of sun protection such as application of sunscreen or wearing protective closing. Funding Sources Almond Board of California.

scholarly journals Luteolin Prevents UVB-Induced Skin Photoaging Damage by Modulating SIRT3/ROS/MAPK Signaling: An in vitro and in vivo Studies

2021 ◽  
Vol 12 ◽  
Author(s):  
Jing Mu ◽  
Huisheng Ma ◽  
Hong Chen ◽  
Xiaoxia Zhang ◽  
Mengyi Ye
Keyword(s):  
Animal Experiments ◽  
Mapk Signaling ◽  
Dermal Fibroblasts ◽  
In Vivo Studies ◽  
Uvb Radiation ◽  
Skin Damage ◽  
Cellular Protection ◽  
Uvb Irradiation

The aim of this study was to investigate the role of luteolin in the mechanism of ultraviolet radiation B (UVB)-induced photoaging. An in vivo photoaging model was established using UVB irradiation of bare skin on the back of rats, and an in vitro photoaging model was established using UVB irradiation of human dermal fibroblasts (HDF). Skin damage was observed using hematoxylin-eosin (HE) and Masson staining, skin and cellular reactive oxygen species (ROS) levels were detected by DHE and DCF fluorescent probes, mitochondrial membrane potential was detected by JC-1 staining, and protein expressions were detected by immunofluorescence and Western Blot. Results from animal experiments showed that luteolin reduced UVB-induced erythema and wrinkle formation. Results from cellular assays showed that luteolin inhibited UVB-induced decrease in cell viability. In addition, in vitro and in vivo experiments showed that luteolin reduced oxidative stress levels, decreased activation of matrix metalloproteinases (MMPs) and increased collagen expression. Continued cellular experiments using 3-TYP, an inhibitor of Sirtuin 3 (SIRT3), revealed a loss of cellular protection by luteolin and a decrease in collagen, suggesting that luteolin acts by targeting and promoting SIRT3. luteolin is involved in the protection of skin cells against UVB radiation-induced ageing via the SIRT3/ROS/mitogen-activated protein kinases (MAPK) axis and it may be a promising therapeutic agent for the prevention of UVB photoaging.

scholarly journals Protective Effect of Vitamin C against Infancy Rat Corneal Injury Caused by Acute UVB Irradiation

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Wei Chen ◽  
Jianying Guo ◽  
Haiyi Guo ◽  
Xue Kong ◽  
Jing Bai ◽  
...  
Keyword(s):  
Vitamin C ◽  
Protective Effect ◽  
Oxidative Status ◽  
Immunofluorescent Staining ◽  
Inflammatory Factors ◽  
Uvb Radiation ◽  
Uvb Irradiation ◽  
Corneal Injury ◽  
Infant Rats ◽  
Uvb Exposure

Purpose. Studies have shown that corneas of young children were more susceptible to Ultraviolet B (UVB) radiation damage. However, there exist limited information about the harm of UVB to eyes and preventive measures on infancy. Vitamin C as an antioxidant is widely used to prevent many diseases. Therefore, the aim of this study was to explore the protective effect of vitamin C on the cornea of infant rats with acute UVB injury. Method. Thirty-six infant rats were randomly divided into three groups: control (CON) group, UVB (UVB) group, and UVB+vitamin C (UVB+VitC) group. The UVB group was exposed to UVB irradiation (8 J/cm2, 15 min/d, 7 d) and the UVB+vitamin C group suffered the same UVB irradiation treated with vitamin C at the dose of 40 mg/kg via intraperitoneal injection. Then, corneal morphology was detected in vivo and in vitro at 7 d post-UVB exposure. Furthermore, serum inflammatory factors (IL-1, IL-6, and TNF-α) and oxidative status (4-HNE and MDA) were detected by ELISA, and the expression of vascular endothelial growth factor-α (VEGF-α) and superoxide dismutase (SOD) in the cornea was detected by western blot or immunofluorescent staining. Results. Slit lamp detection revealed that the area of corneal desquamation and corneal neovascularization in the UVB+VitC group was significantly less than those in the UVB group at 7 d post-UVB exposure (all p<0.05). OCT results showed that the thickness of the central cornea in the UVB+VitC group was decreased than that in the UVB group (p<0.05). The serum inflammatory factors (IL-1, IL-6, and TNF-α) and oxidative status (4-HNE and MDA) in the UVB group were significantly increased compared with the CON group (all p<0.05), while those factors in the UVB+VitC group were decreased compared with those in the UVB group. Furthermore, the expression of VEGF-α in the UVB+VitC group was dramatically decreased compared with that in the UVB group (p<0.05), and the expression of SOD2 in the UVB+VitC group was dramatically increased compared with that in the UVB group at 7 d post-UVB exposure (p<0.05). Conclusion. Vitamin C could protect infant rats from corneal injury induced by UVB via alleviating corneal edema, improving corneal inflammatory reaction, and decreasing VEGF-α expression.

scholarly journals MORIN PREVENTS ULTRAVIOLET-B RADIATION-INDUCED PHOTOCARCINOGENESIS THROUGH ACTIVATING THROMBOSPONDIN-1 IN THE MOUSE SKIN

2018 ◽  
Vol 11 (3) ◽  
pp. 171
Author(s):  
Anjugam C ◽  
Sridevi M ◽  
Rajendra Prasad N ◽  
Agilan Balupillai
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Mouse Skin ◽  
Ultraviolet B ◽  
Uvb Radiation ◽  
Thrombospondin 1 ◽  
Radiation Induced ◽  
Cox 2 ◽  
Uvb Exposure

 Objective: In this study, we investigated whether morin, a natural flavonoid, could able to inhibit ultraviolet B (UVB)-induced carcinogenesis in the skin of Swiss albino mice.Methods: The mice were exposed to UVB radiation (180 mJ/cm2) on weekly thrice for 30 weeks, and morin was administered intraperitoneal and topical application 1 h before UVB exposure. UVB radiation induces the overexpression of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), vascular endothelial growth factor (VEGF), transforming growth factor-beta (TGF-β), and Bcl-2 genes.Results: Morin significantly prevented UVB-induced activation of COX-2, iNOS, VEGF, TGF-β, and Bcl-2 expression in mouse skin. Thrombospondin-1 (TSP), a novel endogenous factor, inhibits angiogenesis and inflammation.Conclusion: The present study illustrates that the protective effect of morin against UVB-induced carcinogenesis may be modulated through activation of TSP-1 in UVB-exposed Swiss albino mice.

scholarly journals Perilla frutescens Extracts Enhance DNA Repair Response in UVB Damaged HaCaT Cells

Nutrients ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 1263
Author(s):  
Hyuna Lee ◽  
Eunmi Park
Keyword(s):  
Antioxidant Activities ◽  
Uv Light ◽  
Mouse Skin ◽  
Perilla Frutescens ◽  
Hacat Cells ◽  
Protective Effects ◽  
Leaf Extracts ◽  
Protein Levels ◽  
Uvb Exposure

Physiological processes in skin are associated with exposure to UV light and are essential for skin maintenance and regeneration. Here, we investigated whether the leaf and callus extracts of Perilla frutescens (Perilla), a well-known Asian herb, affect DNA damage response and repair in skin and keratinocytes exposed to Untraviolet B (UVB) light. First, we examined the protective effects of Perilla leaf extracts in UVB damaged mouse skin in vivo. Second, we cultured calluses using plant tissue culture technology, from Perilla leaf explant and then examined the effects of the leaf and callus extracts of Perilla on UVB exposed keratinocytes. HaCaT cells treated with leaf and callus Perilla extracts exhibited antioxidant activities, smaller DNA fragment tails, and enhanced colony formation after UVB exposure. Interestingly, keratinocytes treated with the leaf and callus extracts of Perilla showed G1/S cell cycle arrest, reduced protein levels of cyclin D1, Cyclin Dependent Kinase 6 (CDK6), and γH2AX, and enhanced levels of phosphorylated checkpoint kinase 1 (pCHK1) following UVB exposure. These observations suggest that the leaf and callus extracts of Perilla are candidate nutraceuticals for the prevention of keratinocyte aging.

scholarly journals Evaluation of Protective Effect of a Water-In-Oil Microemulsion Incorporating Quercetin Against UVB-Induced Damage in Hairless Mice Skin

2010 ◽  
Vol 13 (2) ◽  
pp. 274 ◽  
Author(s):  
Fabiana T. M. C. Vicentini ◽  
Yris M. Fonseca ◽  
Dimitrius L. Pitol ◽  
Mamie M. Iyomasa ◽  
M. Vitória L. B. Bentley ◽  
...  
Keyword(s):  
Topical Application ◽  
Biological Effects ◽  
Elastic Fiber ◽  
Skin Irritation ◽  
Inflammatory Cells ◽  
Protective Effects ◽  
Uvb Radiation ◽  
Hairless Mice ◽  
Uvb Irradiation

Purpose: In the present study, histological aspects were considered in order to evaluate the in vivo photoprotective effect of a w/o microemulsion containing quercetin against UVB irradiation-induced dermal damages. The toxicity in cell culture and the potential skin irritation resulting from topical application of this formulation were also investigated. Methods: Mouse dorsal surfaces were treated topically with 300 mg of the unloaded and quercetin-loaded (0.3%, w/w) microemulsions before and after exposure to UVB (2.87 J/cm2) irradiation. The untreated control groups irradiated and non-irradiated were also evaluated. UVB-induced histopathological changes as well as the photoprotective effect of this formulation were evaluated considering the parameters of infiltration of inflammatory cells, epidermis thickening (basale and spinosum layers) and collagen and elastic fiber contents. The cytotoxicity of the reported formulation was evaluated in L929 mice fibroblasts by MTT assay and the skin irritation was investigated after topical application of both unloaded and quercetin-loaded microemulsions once a day for 15 days. Results: The results demonstrated that the w/o microemulsion containing quercetin reduced the incidence of histological skin alterations, mainly the connective-tissue damage, induced by exposure to UVB irradiation, this allows the suggestion that protective effects of this formulation against UV-induced responses are not secondary to the interference of UV transmission (i.e., blocking the UVB radiation from being absorbed by the skin), as is usually done with UVB absorbers and sunscreens, but is instead due to different biological effects of this flavonoid. Furthermore, by evaluating the cytotoxic effect on L929 cells and histological aspects such as infiltration of inflammatory cells and epidermis thickness of hairless mice, the present study also demonstrated no toxicity of the proposed system. Conclusion: Therefore, based on these mouse models, a detailed characterization of the w/o microemulsion incorporating quercetin effects as a photochemoprotective agent on human skin is thus indicated.

scholarly journals C/EBPα Is a DNA Damage-Inducible p53-Regulated Mediator of the G1 Checkpoint in Keratinocytes

2004 ◽  
Vol 24 (24) ◽  
pp. 10650-10660 ◽  
Author(s):  
Kyungsil Yoon ◽  
Robert C. Smart
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Ataxia Telangiectasia ◽  
P53 Protein ◽  
Mouse Skin ◽  
Uvb Radiation ◽  
Ataxia Telangiectasia Mutated ◽  
Basic Leucine Zipper ◽  
Potent Inducer ◽  
Uvb Irradiation

ABSTRACT The basic leucine zipper transcription factor, CCAAT/enhancer binding protein α (C/EBPα), is abundantly expressed in keratinocytes of the skin; however, its function in skin is poorly characterized. UVB radiation is responsible for the majority of human skin cancers. In response to UVB-induced DNA damage, keratinocytes activate cell cycle checkpoints that arrest cell cycle progression and prevent replication of damaged DNA, allowing time for DNA repair. We report here that UVB radiation is a potent inducer of C/EBPα in human and mouse keratinocytes, as well as in mouse skin in vivo. UVB irradiation of keratinocytes resulted in the transcriptional up-regulation of C/EBPα mRNA, producing a >70-fold increase in C/EBPα protein levels. N-Methyl-N′-nitro-N-nitrosoguanidine, etoposide, and bleomycin also induced C/EBPα. UVB-induced C/EBPα was accompanied by an increase in p53 protein and caffeine, an inhibitor of ataxia-telangiectasia-mutated kinase, and ataxia-telangiectasia-mutated and Rad3-related kinase inhibited UVB-induced increases in both C/EBPα and p53. UVB irradiation of p53-null or mutant p53-containing keratinocytes failed to induce C/EBPα. UVB irradiation of C/EBPα knockdown keratinocytes displayed a greatly diminished DNA damage G1 checkpoint, and this was associated with increased sensitivity to UVB-induced apoptosis. Our results uncover a novel role for C/EBPα as a p53-regulated DNA damage-inducible gene that has a critical function in the DNA damage G1 checkpoint response in keratinocytes.

scholarly journals METTL14 facilitates global genome repair and suppresses skin tumorigenesis

2021 ◽  
Vol 118 (35) ◽  
pp. e2025948118
Author(s):  
Zizhao Yang ◽  
Seungwon Yang ◽  
Yan-Hong Cui ◽  
Jiangbo Wei ◽  
Palak Shah ◽  
...  
Keyword(s):  
Excision Repair ◽  
Mouse Skin ◽  
Dna Lesions ◽  
Ultraviolet B ◽  
Uvb Radiation ◽  
Uvb Irradiation ◽  
Selective Autophagy ◽  
Skin Tumorigenesis ◽  
Global Genome Repair ◽  
Genome Repair

Global genome repair (GGR), a subpathway of nucleotide excision repair, corrects bulky helix-distorting DNA lesions across the whole genome and is essential for preventing mutagenesis and skin cancer. Here, we show that METTL14 (methyltransferase-like 14), a critical component of the N6-methyladenosine (m6A) RNA methyltransferase complex, promotes GGR through regulating m6A mRNA methylation–mediated DDB2 translation and suppresses ultraviolet B (UVB) radiation-induced skin tumorigenesis. UVB irradiation down-regulates METTL14 protein through NBR1-dependent selective autophagy. METTL14 knockdown decreases GGR and DDB2 abundance. Conversely, overexpression of wild-type METTL14 but not its enzymatically inactive mutant increases GGR and DDB2 abundance. METTL14 knockdown decreases m6A methylation and translation of the DDB2 transcripts. Adding DDB2 reverses the GGR repair defect in METTL14 knockdown cells, indicating that METTL14 facilitates GGR through regulating DDB2 m6A methylation and translation. Similarly, knockdown of YTHDF1, an m6A reader promoting translation of m6A-modified transcripts, decreases DDB2 protein levels. Both METTL14 and YTHDF1 bind to the DDB2 transcript. In mice, skin-specific heterozygous METTL14 deletion increases UVB-induced skin tumorigenesis. Furthermore, METTL14 as well as DDB2 is down-regulated in human and mouse skin tumors and by chronic UVB irradiation in mouse skin, and METTL14 level is associated with the DDB2 level, suggesting a tumor-suppressive role of METTL14 in UVB-associated skin tumorigenesis in association with DDB2 regulation. Taken together, these findings demonstrate that METTL14 is a target for selective autophagy and acts as a critical epitranscriptomic mechanism to regulate GGR and suppress UVB-induced skin tumorigenesis.

scholarly journals On-person adaptive evolution of Staphylococcus aureus during atopic dermatitis increases disease severity

2021 ◽  
Author(s):  
Felix M. Key ◽  
Veda D. Khadka ◽  
Carolina Romo-González ◽  
Kimbria J. Blake ◽  
Liwen Deng ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Atopic Dermatitis ◽  
Disease Severity ◽  
De Novo ◽  
Mouse Skin ◽  
The Body ◽  
Single Mutation ◽  
Skin Damage ◽  
Adaptive Mutations

Bacteria acquire adaptive mutations during infections and within healthy microbiomes 1-4, but the potential of bacterial mutations to impact disease is not well understood. The inflamed skin of people with atopic dermatitis (AD) is heavily colonized with Staphylococcus aureus, an opportunistic pathogen associated with both asymptomatic colonization of nasal passages and invasive disease5,6. While host genetic risk is critical to AD initiation 7,8, S. aureus worsens disease severity by inducing skin damage9. Here, we longitudinally track S. aureus evolution on 25 children with AD over 9 months —sequencing the genomes of 1,330 colonies— and identify common adaptive de novo mutations that exacerbate skin disease in vivo. Novel S. aureus genotypes replace their ancestors across the body within months, with signatures of adaptive, rather than neutral, forces. Most strikingly, the capsule synthesis gene capD obtained four parallel mutations within one patient and is involved in mutational sweeps in multiple patients. Despite the known role of capsule in phagocytic evasion10, we find that an acapsular ΔcapD strain colonizes better and produces worse disease severity on mouse skin than its encapsulated parental strain. Moreover, re-analysis of publicly available S. aureus genomes from 276 people confirms that CapD truncations are significantly more common among strains isolated from AD patients relative to other contexts. Together, these results suggest that targeting capsule-negative strains may be a potential avenue for decreasing S. aureus skin colonization and highlight the importance of single-mutation resolution for characterizing microbe-disease associations.

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