scholarly journals Protective Effects of Sesamin Against UVB-Induced Skin Inflammation and Photodamage In Vitro and In Vivo

Biomolecules ◽  
2019 ◽  
Vol 9 (9) ◽  
pp. 479 ◽  
Author(s):  
Lin ◽  
Wu ◽  
Hou ◽  
Chien ◽  
Chang ◽  
...  
Keyword(s):  
Protein Expression ◽  
Map Kinase ◽  
Human Fibroblasts ◽  
Mouse Skin ◽  
P38 Map Kinase ◽  
Dermal Fibroblasts ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Protective Effects ◽  
Cox 2

Ultraviolet (UV) exposure has been demonstrated as the most critical factor causing extrinsic skin aging and inflammation. This study explored the protective effects and mechanisms of sesamin against skin photodamage. Sesamin reduced intracellular reactive oxygen species production after UVB irradiation in human dermal fibroblasts. The sesamin treatment attenuated mitogen-activated protein (MAP) kinase phosphorylation and matrix metalloproteinase (MMPs) overexpression induced by UVB exposure, and it significantly enhanced the tissue inhibitor of metalloproteinase-1 protein expression. Sesamin also elevated the total collagen content in human fibroblasts by inhibiting UVB-induced mothers against decapentaplegic homolog 7 (Smad7) protein expression. Sesamin reduced UVB-induced inducible nitric oxide synthase (i-NOS) and cyclooxygenase-2 (COX-2) overexpression and inhibited nuclear factor-kappa B (NF-κB) translocation. Moreover, sesamin may regulate the c-Jun N-terminal kinases (JNK) and p38 MAP kinase pathways, which inhibit COX-2 expression. Sesamin could reduce UVB-induced inflammation, epidermal hyperplasia, collagen degradation, and wrinkle formation in hairless mice. It also reduced MMP-1, interleukin (IL-1), i-NOS, and NF-κB in the mouse skin. These results demonstrate that sesamin had antiphotodamage and anti-inflammatory activities. Sesamin has potential for use as a skin protection agent in antiphotodamage and skin care products.

scholarly journals Creatine and Nicotinamide Prevent Oxidant-Induced Senescence in Human Fibroblasts

Nutrients ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 4102
Author(s):  
Avinash S. Mahajan ◽  
Venkata S. Arikatla ◽  
Anita Thyagarajan ◽  
Tetyana Zhelay ◽  
Ravi P. Sahu ◽  
...  
Keyword(s):  
Protein Expression ◽  
Human Fibroblasts ◽  
Reactive Oxygen Species Generation ◽  
Dermal Fibroblasts ◽  
Ultraviolet B ◽  
Epidermal Keratinocytes ◽  
Mrna Levels ◽  
H2o2 Treatment ◽  
Structural Support

Dermal fibroblasts provide structural support by producing collagen and other structural/support proteins beneath the epidermis. Fibroblasts also produce insulin-like growth factor-1 (IGF-1), which binds to the IGF-1 receptors (IGF-1Rs) on keratinocytes to activate signaling pathways that regulate cell proliferation and cellular responses to genotoxic stressors like ultraviolet B radiation. Our group has determined that the lack of IGF-1 expression due to fibroblast senescence in the dermis of geriatric individuals is correlated with an increased incidence of skin cancer. The present studies tested the hypothesis that pro-energetics creatine monohydrate (Cr) and nicotinamide (NAM) can protect normal dermal human fibroblasts (DHF) against experimentally induced senescence. To that end, we used an experimental model of senescence in which primary DHF are treated with hydrogen peroxide (H2O2) in vitro, with senescence measured by staining for beta-galactosidase activity, p21 protein expression, and senescence associated secretory phenotype cytokine mRNA levels. We also determined the effect of H2O2 on IGF-1 mRNA and protein expression. Our studies indicate that pretreatment with Cr or NAM protects DHF from the H2O2-induced cell senescence. Treatment with pro-energetics post-H2O2 had no effect. Moreover, these agents also inhibited reactive oxygen species generation from H2O2 treatment. These studies suggest a potential strategy for protecting fibroblasts in geriatric skin from undergoing stress-induced senescence, which may maintain IGF-1 levels and therefore limit carcinogenesis in epidermal keratinocytes.

Bile acids stimulate PKCα autophosphorylation and activation: role in the attenuation of prostaglandin E1-induced cAMP production in human dermal fibroblasts

2006 ◽  
Vol 291 (2) ◽  
pp. G275-G287 ◽  
Author(s):  
Man Le ◽  
Lada Krilov ◽  
Jianping Meng ◽  
Kelli Chapin-Kennedy ◽  
Susan Ceryak ◽  
...  
Keyword(s):  
Bile Acid ◽  
Map Kinase ◽  
Bile Acids ◽  
P38 Map Kinase ◽  
Dermal Fibroblasts ◽  
Dominant Negative ◽  
Human Dermal Fibroblasts ◽  
Camp Production ◽  
Acid Effect

The aim was to identify the specific PKC isoform(s) and their mechanism of activation responsible for the modulation of cAMP production by bile acids in human dermal fibroblasts. Stimulation of fibroblasts with 25–100 μM of chenodeoxycholic acid (CDCA) and ursodeoxycholic acid (UDCA) led to YFP-PKCα and YFP-PKCδ translocation in 30–60 min followed by a transient 24- to 48-h downregulation of the total PKCα, PKCδ, and PKCε protein expression by 30–50%, without affecting that of PKCζ. Increased plasma membrane translocation of PKCα was associated with an increased PKCα phosphorylation, whereas increased PKCδ translocation to the perinuclear domain was associated with an increased accumulation of phospho-PKCδ Thr505 and Tyr311 in the nucleus. The PKCα specificity on the attenuation of cAMP production by CDCA was demonstrated with PKC downregulation or inhibition, as well as PKC isoform dominant-negative mutants. Under these same conditions, neither phosphatidylinositol 3-kinase, p38 MAP kinase, p42/44 MAP kinase, nor PKA inhibitors had any significant effect on the CDCA-induced cAMP production attenuation. CDCA concentrations as low as 10 μM stimulated PKCα autophosphorylation in vitro. This bile acid effect required phosphatidylserine and was completely abolished by the presence of Gö6976. CDCA at concentrations less than 50 μM enhanced the PKCα activation induced by PMA, whereas greater CDCA concentrations reduced the PMA-induced PKCα activation. CDCA alone did not affect PKCα activity in vitro. In conclusion, although CDCA and UDCA activate different PKC isoforms, PKCα plays a major role in the bile acid-induced inhibition of cAMP synthesis in fibroblasts. This study emphasizes potential consequences of increased systemic bile acid concentrations and cellular bile acid accumulation in extrahepatic tissues during cholestatic liver diseases.

scholarly journals [6]-Gingerol inhibits COX-2 expression by blocking the activation of p38 MAP kinase and NF-κB in phorbol ester-stimulated mouse skin

Oncogene ◽  
2005 ◽  
Vol 24 (15) ◽  
pp. 2558-2567 ◽  
Author(s):  
Sue Ok Kim ◽  
Joydeb Kumar Kundu ◽  
Young Kee Shin ◽  
Jin-Hong Park ◽  
Myung-Haing Cho ◽  
...  
Keyword(s):  
Map Kinase ◽  
Phorbol Ester ◽  
Mouse Skin ◽  
P38 Map Kinase ◽  
Cox 2

scholarly journals 1,2-Bis[(3-Methoxyphenyl)Methyl]Ethane-1,2-Dicarboxylic Acid Reduces UVB-Induced Photodamage In Vitro and In Vivo

Antioxidants ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 452 ◽  
Author(s):  
Wu ◽  
Lin ◽  
Hou ◽  
Chang ◽  
Wen ◽  
...  
Keyword(s):  
Protein Expression ◽  
Dicarboxylic Acid ◽  
Map Kinases ◽  
Mouse Skin ◽  
Dermal Fibroblasts ◽  
Premature Aging ◽  
Activator Protein 1 ◽  
Anti Inflammatory

This study investigated the effects and mechanisms of 1,2-bis[(3-methoxyphenyl)methyl]ethane-1,2-dicarboxylic acid (S4), a sesamin derivative, on anti-inflammation and antiphotoaging in vitro and in vivo. Human skin fibroblasts were treated with S4 and did not show cytotoxicity under concentrations of 5–50 µM. In addition, S4 also reduced ultraviolet (UV)B-induced intracellular reactive oxygen species (ROS) production. Additionally, S4 inhibited UVB-induced phosphorylation of mitogen-activated protein (MAP) kinases, activator protein-1 (AP-1), and matrix metalloproteinases (MMPs) overexpression. Furthermore, S4 also inhibited UVB-induced Smad7 protein expression and elevated total collagen content in human dermal fibroblasts. For anti-inflammatory activity, S4 inhibited UVB-induced nitric oxide synthase (i-NOS) and cyclooxygenase (COX)-2 protein expression and inhibited nuclear factor-kappaB (NF-ĸB) translocation into the nucleus. S4 ameliorated UVB-induced erythema and wrinkle formation in hairless mice. On histological observation, S4 also ameliorated UVB-induced epidermal hyperplasia and collagen degradation. S4 reduced UVB-induced MMP-1, interleukin (IL)-6, and NF-ĸB expression in the mouse skin. The results indicated that S4 had antiphotoaging and anti-inflammatory activities, protecting skin from premature aging.

scholarly journals Combined Effects of Carotenoids and Polyphenols in Balancing the Response of Skin Cells to UV Irradiation

Molecules ◽  
2021 ◽  
Vol 26 (7) ◽  
pp. 1931
Author(s):  
Glenda Calniquer ◽  
Marina Khanin ◽  
Hilla Ovadia ◽  
Karin Linnewiel-Hermoni ◽  
David Stepensky ◽  
...  
Keyword(s):  
Cell Damage ◽  
Plasma Concentrations ◽  
Dermal Fibroblasts ◽  
Carnosic Acid ◽  
Rosemary Extract ◽  
Protective Effects ◽  
Skin Cells ◽  
Tomato Extract ◽  
Clinical Experiments

Oral carotenoids and polyphenols have been suggested to induce photo-protective effects. The aim of the study was to test whether the combination of carotenoids and polyphenols produce greater protective effects from UV-induced damage to skin cells. Such damage is characterized by inflammation and oxidative stress; thus, the photo-protective effect can be partially explained by modulating the nuclear factor kappa B (NFκB) and antioxidant response element/Nrf2 (ARE/Nrf2) transcription systems, known as important regulators of these two processes. Indeed, it was found in keratinocytes that carotenoids and polyphenols inhibit UVB-induced NFκB activity and release of cytokine IL-6. A combination of tomato extract with rosemary extract inhibited UVB-induced release of IL-6 more than each of the compounds alone. Moreover, this combination synergistically activated ARE/Nrf2 transcription systems. Inflammatory cytokines such as IL-6 and TNFα induce the expression of matrix metalloproteinases (MMPs), which leads to collagen breakdown; thus, it is important to note that carnosic acid reduced TNFα-induced MMP-1 secretion from human dermal fibroblasts. The in vitro results suggest beneficial effects of phytonutrient combinations on skin health. To assure that clinical experiments to prove such effects in humans are feasible, the human bioavailability of carotenoids from tomato extract was tested, and nearly a twofold increase in their plasma concentrations was detected. This study demonstrates that carotenoids and polyphenols cooperate in balancing UV-induced skin cell damage, and suggests that NFκB and ARE/Nrf2 are involved in these effects.

Boswellia serrata oleo-gum-resin and β-boswellic acid inhibits HSV-1 infection in vitro through modulation of NF-кB and p38 MAP kinase signaling

Phytomedicine ◽  
2018 ◽  
Vol 51 ◽  
pp. 94-103 ◽  
Author(s):  
Debayan Goswami ◽  
Ananya Das Mahapatra ◽  
Subhadip Banerjee ◽  
Amit Kar ◽  
Durbadal Ojha ◽  
...  
Keyword(s):  
Map Kinase ◽  
P38 Map Kinase ◽  
Kinase Signaling ◽  
Boswellic Acid ◽  
Boswellia Serrata ◽  
Map Kinase Signaling ◽  
Hsv 1

scholarly journals Differential role of cAMP, cGMP and Ca2+ and involvement of kinases and CBP-CREB-CRE pathway in regulation of arylalkylamine N-acetyltransferase 2 gene in the pineal organ of air-breathing catfish, Clarias gariepinus

2021 ◽  
Author(s):  
Hijam Nonibala ◽  
Braj Bansh Prasad Gupta
Keyword(s):  
Gene Expression ◽  
Map Kinase ◽  
Gene Transcription ◽  
Pineal Organ ◽  
Clarias Gariepinus ◽  
Specific Inhibitor ◽  
P38 Map Kinase ◽  
Camp And Cgmp

Abstract Transcription of arylalkylamine N-acetyltransferase 2 (aanat2) gene leads to formation of AANAT2 - the rate-limiting enzyme in melatonin synthesis pathway in photosensitive fish pineal organ. However, unlike in avian and mammalian pineal gland, there is practically no information on signal transduction pathway(s) involved in regulation of aanat2 gene transcription in the fish pineal organ. Therefore, we investigated the role of important molecular components of signalling via cAMP, cGMP, Ca2+ involving PKA, PKG, PKC, MeK and p38 MAP kinase as well as possible role of serine/threonine phosphatases, CREB and CBP using their specific inhibitors and/or activators in aanat2 gene transcription in the fish pineal organ maintained under in vitro culture-conditions. db-cAMP and db-cGMP stimulated the expression of aanat2 gene. db-cAMP- and cGMP-induced aanat2 gene expression was significantly reduced in the presence of H-89 (specific inhibitor of PKA), KT5823 (specific inhibitor of PKG), chelerythrine chloride (specific inhibitor of PKC), U0126 ethanolate (specific inhibitor of MeK) and SB 202190 monohydrochloride hydrate (specific inhibitor of p38 MAP kinase). Inhibitors of PP1 and PP2A significantly increased aanat2 gene expression as well as significantly reduced cAMP- and cGMP-induced gene transcription, while inhibitor of PP2B had no effect on aanat2 gene expression. Inhibitors of both CREB and CBP-CREB interaction completely blocked cAMP-induced aanat2 gene transcription. Based on these findings, we suggest that cAMP, cGMP and Ca2+ stimulate aanat2 gene transcription via PKA, PKG and PKC, respectively. Further, protein phosphatases and CBP-CREB-CRE pathway are actively involved in regulation of on aanat2 gene expression in the fish pineal organ.

scholarly journals The Activity of Combination of Hydrolyzed Virgin Coconut Oil and Chitosan Toward Wound Healing Parameters on NIH 3T3 Cells Using in Vitro Methods

1970 ◽  
Vol 7 (3) ◽  
pp. 14-19 ◽  
Author(s):  
Hekdin Marsius Sipayung ◽  
Jansen Silalahi ◽  
Yuandani Y
Keyword(s):  
Cell Proliferation ◽  
Wound Healing ◽  
Protein Expression ◽  
Scratch Wound ◽  
Cell Proliferation Activity ◽  
Proliferation Activity ◽  
Cox 2 ◽  
Nih 3T3 ◽  
Vegf Protein

Objectives: The objective of this study was to investigate the activity of combination of hydrolyzed VCO (HVCO) and chitosan on NIH 3T3 cell proliferation activity, NIH 3T3 cell migration, COX-2 and VEGF protein expression. Design: In vitro cytotoxic assay was determined by MTT (MicrocultureTetrazoliumTehnique) assay, cell proliferation activity was measured by calculating cell viability incubated 24 hours, 48 hours and 72 hours, wound closure percentage was tested by scratch wound healing method, expression of COX-2 protein and VEGF protein were measured by immunocytochemical method. Interventions: The variable that was intervened in this study was the concentration of HVCO and chitosan. Main Outcome Measures: The main measurements carried out in this study were the absorbance value of HVCO and chitosan which was converted into viability cell, proliferation activity, percentage of wound closure, and percentage of COX-2 and VEGF protein expression. Results: Cytotoxic activity of HVCO and chitosan resulted the best concentration at 31.25 μg/ml, scratch wound healing assay from a combination HVCO and chitosan resulted the best migration of fibroblast cells at a ratio of 1:1 with HVCO 62.5 μg/ml and chitosan 62.5 μg/ml, combination of HVCO 62.5 μg/ml and chitosan 62.5 μg/ml (1:1) increased expression of COX-2 and VEGF. Conclusion: Combination of HVCO and chitosan could increase NIH 3T3 cell migration, COX-2 and VEGF protein expression. Combination of HVCO and chitosan had better wound healing activity in vitro than single use. Keywords: Rhizomucor miehei, viability, proliferation, migration, expression

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