Glycolic acid attenuates UVB-induced aquaporin-3, matrix metalloproteinase-9 expression, and collagen degradation in keratinocytes and mouse skin

2019 ◽  
Vol 476 (10) ◽  
pp. 1387-1400 ◽  
Author(s):  
Sheau-Chung Tang ◽  
Lee-Chun Tang ◽  
Chin-Hung Liu ◽  
Pei-Yun Liao ◽  
Ji-Ching Lai ◽  
...  
Keyword(s):  
Glycolic Acid ◽  
Transient Receptor Potential ◽  
Mouse Skin ◽  
Skin Aging ◽  
Ultraviolet B ◽  
Mitogen Activated Protein Kinase ◽  
Transient Receptor Potential Vanilloid ◽  
Type I ◽  
Dorsal Skin ◽  
Aquaporin 3

Abstract Ultraviolet-B exposure causes an inflammatory response, photoaged skin, and degradation of extracellular matrix proteins including collagen and elastin. The regulation of these genes was suggested as an important mechanism to attenuate skin aging. Glycolic acid (GA) is commonly present in fruits and recently used to treat dermatological diseases. We reported that GA slows down cell inflammation and aging caused by UVB. Little is known about GA retarding the skin premature senescence or how to impede these events. To investigate the potential of GA to regulate the expression of MMPs and collagen, GA was topically applied onto human keratinocytes and the C57BL/6J mice dorsal skin. In the present study, we demonstrated that GA reduced UVB-induced type-I procollagen expression and secretory collagen levels. GA reverted and dose-dependently increased the level of aquaporin-3 (AQP3), the expression of which was down-regulated by UVB. The UV-induced MMP-9 level and activity were reduced by GA pre-treatment. Concomitantly, GA reverted mitogen-activated protein kinase (MMP-9) activation and inhibited the extracellular signal-regulated kinase activation (p38, pERK) triggered by UVB. The animal model also presented that GA attenuated the wrinkles caused by UVB on the mouse dorsal skin. Finally, GA triggers the transient receptor potential vanilloid-1 (TRPV-1) channel to initiate the anti-photoaging mechanism in keratinocytes. These findings clearly indicated that the mechanisms of GA promote skin protection against UVB-induced photoaging and wrinkle formation. GA might be an important reagent and more widely used to prevent UVB-induced skin aging.

scholarly journals TRPV1 promotes opioid analgesia during inflammation

2019 ◽  
Vol 12 (575) ◽  
pp. eaav0711 ◽  
Author(s):  
Lilian Basso ◽  
Reem Aboushousha ◽  
Churmy Yong Fan ◽  
Mircea Iftinca ◽  
Helvira Melo ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Opioid Receptor ◽  
Inflammatory Pain ◽  
Transient Receptor Potential ◽  
Nuclear Translocation ◽  
Mapk Signaling ◽  
Mitogen Activated Protein Kinase ◽  
Opioid Analgesia ◽  
Transient Receptor Potential Vanilloid ◽  
Receptor Desensitization

Pain and inflammation are inherently linked responses to injury, infection, or chronic diseases. Given that acute inflammation in humans or mice enhances the analgesic properties of opioids, there is much interest in determining the inflammatory transducers that prime opioid receptor signaling in primary afferent nociceptors. Here, we found that activation of the transient receptor potential vanilloid type 1 (TRPV1) channel stimulated a mitogen-activated protein kinase (MAPK) signaling pathway that was accompanied by the shuttling of the scaffold protein β-arrestin2 to the nucleus. The nuclear translocation of β-arrestin2 in turn prevented its recruitment to the μ-opioid receptor (MOR), the subsequent internalization of agonist-bound MOR, and the suppression of MOR activity that occurs upon receptor desensitization. Using the complete Freund’s adjuvant (CFA) inflammatory pain model to examine the role of TRPV1 in regulating endogenous opioid analgesia in mice, we found that naloxone methiodide (Nal-M), a peripherally restricted, nonselective, and competitive opioid receptor antagonist, slowed the recovery from CFA-induced hypersensitivity in wild-type, but not TRPV1-deficient, mice. Furthermore, we showed that inflammation prolonged morphine-induced antinociception in a mouse model of opioid receptor desensitization, a process that depended on TRPV1. Together, our data reveal a TRPV1-mediated signaling pathway that serves as an endogenous pain-resolution mechanism by promoting the nuclear translocation of β-arrestin2 to minimize MOR desensitization. This previously uncharacterized mechanism may underlie the peripheral opioid control of inflammatory pain. Dysregulation of the TRPV1–β-arrestin2 axis may thus contribute to the transition from acute to chronic pain.

scholarly journals Inhibitory Effect of Manassantin B Isolated from Saururus chinensis on Skin Heat Aging

Cosmetics ◽  
2020 ◽  
Vol 7 (2) ◽  
pp. 47
Author(s):  
Hwa Sun Ryu ◽  
Jeong-Yeon Choi ◽  
Kyeong-Sun Lee ◽  
Jung-No Lee ◽  
Chun Mong Lee ◽  
...  
Keyword(s):  
Heat Shock ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Skin Aging ◽  
Shock Treatment ◽  
Transient Receptor Potential Vanilloid ◽  
Dependent Manner ◽  
Heat Shock Treatment ◽  
Channel Inhibition ◽  
Saururus Chinensis

Heat shock treatment-induced skin aging causes a thickened epidermis, increased matrix metalloproteinase (MMP)-1 expression, collagen degradation, and deep wrinkles. In this study, we investigated the effect of manassantin B in preventing heat shock treatment-induced aging. We first separated manassantin B (MB) from the roots of Saururus chinensis, and the structure was identified using 1H- and 13C-NMR spectroscopy. RT-PCR and western blotting were applied to investigate the anti-aging effect of manassantin B. Manassantin B decreased MMP-1 expression through transient receptor potential vanilloid (TRPV) 1 channel inhibition and significantly increased procollagen expression. In addition, manassantin B suppressed MAPK phosphorylation in a dose-dependent manner. Our results suggest that manassantin B, the active ingredient in S. chinensis, can be effectively used to inhibit heat shock treatment-induced skin aging.

scholarly journals Investigating the Multitarget Mechanism of Traditional Chinese Medicine Prescription for Cancer-Related Pain by Using Network Pharmacology and Molecular Docking Approach

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Jinyuan Chang ◽  
Lixing Liu ◽  
Yaohan Wang ◽  
Yutong Sui ◽  
Hao Li ◽  
...  
Keyword(s):  
Molecular Docking ◽  
Transient Receptor Potential ◽  
Trp Channels ◽  
Receptor Potential ◽  
Binding Activity ◽  
Mitogen Activated Protein Kinase ◽  
Network Pharmacology ◽  
Transient Receptor Potential Vanilloid ◽  
Mitogen Activated Protein ◽  
Transient Receptor

Gu-tong formula (GTF) has achieved good curative effects in the treatment of cancer-related pain. However, its potential mechanisms have not been explored. We used network pharmacology and molecular docking to investigate the molecular mechanism and the effective compounds of the prescription. Through the analysis and research in this paper, we obtained 74 effective compounds and 125 drug-disease intersection targets to construct a network, indicating that quercetin, kaempferol, and β-sitosterol were possibly the most important compounds in GTF. The key targets of GTF for cancer-related pain were Jun proto-oncogene (JUN), mitogen-activated protein kinase 1 (MAPK1), and RELA proto-oncogene (RELA). 2204 GO entries and 148 pathways were obtained by GO and KEGG enrichment, respectively, which proved that chemokine, MAPK, and transient receptor potential (TRP) channels can be regulated by GTF. The results of molecular docking showed that stigmasterol had strong binding activity with arginine vasopressin receptor 2 (AVPR2) and C-X3-C motif chemokine ligand 1 (CX3CL1) and cholesterol was more stable with p38 MAPK, prostaglandin-endoperoxide synthase 2 (PTGS2), and transient receptor potential vanilloid-1 (TRPV1). In conclusion, the therapeutic effect of GTF on cancer-related pain is based on the comprehensive pharmacological effect of multicomponent, multitarget, and multichannel pathways. This study provides a theoretical basis for further experimental research in the future.

scholarly journals Topical Application of Aronia melanocarpa Extract Rich in Chlorogenic Acid and Rutin Reduces UVB-Induced Skin Damage via Attenuating Collagen Disruption in Mice

Molecules ◽  
2020 ◽  
Vol 25 (19) ◽  
pp. 4577
Author(s):  
Young Her ◽  
Tae-Kyeong Lee ◽  
Jong Dai Kim ◽  
Bora Kim ◽  
Hyejin Sim ◽  
...  
Keyword(s):  
Chlorogenic Acid ◽  
High Performance ◽  
Collagen Type ◽  
Collagen Type I ◽  
Ultraviolet B ◽  
Type I ◽  
Protective Effects ◽  
Dorsal Skin ◽  
Skin Damage ◽  
Aronia Melanocarpa

Aronia melanocarpa, a black chokeberry, contains high levels of phenolic acids and polyphenolic flavonoids and displays antioxidative and anti-inflammatory effects. Through high-performance liquid chromatography for extracts from Aronia melanocarpa, we discovered that the extract contained chlorogenic acid and rutin as major ingredients. In this study, we examined the protective effects of the extract against ultraviolet B- (UVB)-induced photodamage in the dorsal skin of institute of cancer research (ICR) mice. Their dorsal skin was exposed to UVB, thereafter; the extract was topically applied once a day for seven days. Photoprotective properties of the extract in the dorsal skin were investigated by clinical skin severity score for skin injury, hematoxylin and eosin staining for histopathology, Masson’s trichrome staining for collagens. In addition, we examined change in collagen type I and III, and matrix metalloproteinase (MMP)-1 and MMP-3 by immunohistochemistry. In the UVB-exposed mice treated with the extract, UVB-induced epidermal damage was significantly ameliorated, showing that epidermal thickness was moderated. In these mice, immunoreactivities of collagen type I and III were significantly increased, whereas immunoreactivities of MMP-1 and 3 were significantly decreased compared with those in the UVB-exposed mice. These results indicate that treatment with Aronia melanocarpa extract attenuates UV-induced photodamage by attenuating UVB-induced collagen disruption: these findings might be a result of the chlorogenic acid and rutin contained in the extract. Based on the current results, we suggest that Aronia melanocarpa can be a useful material for developing photoprotective adjuvant.

Dermal Histology in Mouse Skin Exposed to Cosmeceuticals

2017 ◽  
Vol 33 (05) ◽  
pp. 545-550
Author(s):  
Hope Bueller ◽  
Yvonne Hsia ◽  
J. Thomas ◽  
Tapan Bhattacharyya
Keyword(s):  
Quantitative Data ◽  
Chronic Exposure ◽  
Glycolic Acid ◽  
Mouse Skin ◽  
Hairless Mouse ◽  
Dorsal Skin ◽  
Histopathological Changes ◽  
Over The Counter ◽  
Aging Populations ◽  
Skin Samples

AbstractChronic exposure to environmental ultraviolet radiation elicits deleterious photoaging changes and histopathological damage to the skin. In addition to cosmetic surgical procedures, over-the-counter products described as cosmeceuticals are widely used by a large segment of globally aging populations to partially reverse changes induced by photoaging. Many such products are rarely examined in the laboratory to examine their ameliorative properties and microscopic effects on various skin compartments. The hairless mouse is a popular animal model widely used over the last few decades by researchers to compare cosmeceuticals about their properties to combat or reverse cutaneous photoaging changes. In the present experiment, five cosmeceuticals were topically administered to the dorsal skin over 2 weeks in the nonirradiated mice, and skin samples were analyzed for dermal histopathological changes. Histomorphometric procedures were employed to generate quantitative data on skin sections prepared with immunohistochemistry and staining technics, and the data statistically examined. Among the five agents tested, glycolic acid and retinoic acid produced striking changes, while vitamin C, estrogen, and soy product resulted in less remarkable responses. These quantitative data will be useful for further photoaging studies with these cosmeceuticals.

scholarly journals Protective Effect of Polymethoxyflavones Isolated from Kaempferia parviflora against TNF-α-Induced Human Dermal Fibroblast Damage

Antioxidants ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 1609
Author(s):  
Hung Manh Phung ◽  
Sullim Lee ◽  
Sukyung Hong ◽  
Sojung Lee ◽  
Kiwon Jung ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Responses ◽  
Skin Aging ◽  
Dermal Fibroblasts ◽  
Mitogen Activated Protein Kinase ◽  
Type I ◽  
Skin Damage ◽  
Kaempferia Parviflora ◽  
Matrix Metalloproteinase 1 ◽  
Tnf Α

Similar to other organs, the skin undergoes a natural aging process. Moreover, constant direct exposure to environmental stresses, including ultraviolet irradiation, causes the signs of skin aging to appear rather early. Reactive oxygen species (ROS) and inflammatory responses accelerate skin damage in extrinsic aging. In this study, we aimed to investigate the skin protective effects of polymethoxyflavones found in Kaempferia parviflora against oxidative stress and inflammation-induced damage in human dermal fibroblasts (HDFs) stimulated by tumor necrosis factor-α (TNF-α). The experimental data identified 5,7,4′ trimethoxyflavone (TMF) as the most potent constituent in preventing TNF-α-induced HDF damage among the tested compounds and it was not only effective in inhibiting matrix metalloproteinase-1 (MMP-1) production but also in stimulating collagen, type I, and alpha 1 (COLIA1) expression. TMF suppressed TNF-α-stimulated generation of ROS and pro-inflammatory mediators, such as cyclooxygenase-2 (COX-2), interleukin (IL)-1β, and IL-6 in HDFs. TMF also inhibited the pathways regulating fibroblast damage, including mitogen-activated protein kinase (MAPK), activator protein 1 (AP-1), and nuclear factor-kappa B (NF-κB). In conclusion, TMF may be a potential agent for preventing skin aging and other dermatological disorders associated with oxidative stress and inflammation.

scholarly journals Effect of Lactobacillus reuteri Administration on Wrinkle Formation and Type I Procollagen Levels in UVB-Exposed Male Balb/c Mice (Mus musculus)

2020 ◽  
Vol 4 (3) ◽  
pp. 113
Author(s):  
Ivanna Valentina ◽  
Achadiyani Achadiyani ◽  
Sunarjati Sudigdo Adi ◽  
Ronny Lesmana ◽  
Reni Farenia
Keyword(s):  
Oxidative Stress ◽  
Lactobacillus Reuteri ◽  
Ultraviolet B ◽  
Type I ◽  
Uvb Radiation ◽  
Dorsal Skin ◽  
Uvb Irradiation ◽  
Type I Procollagen ◽  
Group 3 ◽  
Group 1

Background: Chronic Ultraviolet B (UVB) exposure causes oxidative stress that may induce damages to the collagen matrix and thus plays a role in the wrinkle formation. Lactobacillus reuteri is a probiotic that may exerts antioxidant effects, thus helping to reduce damages caused by UVB-induced oxidative stress in the skin.Materials and Methods: Twenty-eight male Balb/c mice were divided equally into control group, UVB radiation only group, oral L. reuteri supplementation only group, and UVB radiation with oral L. reuteri supplementation group. UVB irradiation was given 3 times a week (100 seconds/exposure, within 3 cm distance) for 10 weeks, with a total dose of 166 mJ/cm2. Oral L. reuteri supplementation (0.2 mL, 108 CFU) was provided every morning after meal via orogastric feeding tube for 10 weeks. Wrinkle formation on the dorsal skin of the mice was evaluated in accordance with the Bissett method and type I procollagen levels was evaluated by western blotting.Results: In comparison with the group receiving only UVB irradiation, the group receiving probiotic and UVB irradiation showed significantly lower wrinkle scores (Group 1 vs. Group 3, 2.50±0.55 vs. 1.00±0,00; p<0.05) and significantly higher type I procollagen levels (Group 1 vs. Group 3, 0.88±0.36 vs. 1.92±0.46; p<0.05).Conclusion: Results of the current study showed that L. reuteri supplementation may reduce wrinkle formation and increase type I procollagen production in UVB-exposed dorsal skin of male Balb/c mice.Keywords: Lactobacillus reuteri, type I procollagen, photoaging, wrinkles, ultraviolet B

scholarly journals Photoprotective Effects of a Hyperoside-Enriched Fraction Prepared from Houttuynia cordata Thunb. on Ultraviolet B-Induced Skin Aging in Human Fibroblasts through the MAPK Signaling Pathway

Plants ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 2628
Author(s):  
Sariya Mapoung ◽  
Sonthaya Umsumarng ◽  
Warathit Semmarath ◽  
Punnida Arjsri ◽  
Kamonwan Srisawad ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Human Fibroblasts ◽  
Mapk Signaling ◽  
Skin Aging ◽  
Dermal Fibroblasts ◽  
Mapk Signaling Pathway ◽  
Ultraviolet B ◽  
Type I ◽  
Houttuynia Cordata ◽  
Houttuynia Cordata Thunb

Ultraviolet-B (UVB) irradiation causes skin damage via deleterious effects including oxidative stress, inflammation, and collagen degradation. The photoprotective effects of a hyperoside-enriched fraction obtained from Houttuynia cordata Thunb. (H. cordata) on the attenuation of UVB-induced skin aging in human fibroblasts were investigated. The solvent-partition technique was used to establish the hyperoside-enriched fraction of H. cordata (HcEA). The active compounds identified in the H. cordata extracts were hyperoside, quercitrin, chlorogenic acid, and rutin. With regard to the photoprotective effects of H. cordata on UVB-irradiated dermal fibroblasts, HcEA and hyperoside inhibited intracellular ROS production and inflammatory cytokine secretions (IL-6 and IL-8), while increasing collagen type I synthesis along with downregulating MMP-1 gene and protein expressions. Mechanistically, the hyperoside-enriched fraction obtained from H. cordata inhibited UVB-irradiated skin aging through regulation of the MAPK signaling pathway by attenuating the activation of JNK/ERK/c-Jun in human dermal fibroblasts. The hyperoside-enriched fraction of H. cordata exerted potent anti-skin aging properties against UVB exposure. The findings of this study can be applied in the cosmetics industry, as H. cordata extract can potentially be used in pharmaceutical or cosmetic formulations as a photoprotective or anti-skin aging agent.

scholarly journals The Lipoxin Receptor/FPR2 Agonist BML-111 Protects Mouse Skin Against Ultraviolet B Radiation

Molecules ◽  
2020 ◽  
Vol 25 (12) ◽  
pp. 2953
Author(s):  
Renata M. Martinez ◽  
Victor Fattori ◽  
Priscila Saito ◽  
Ingrid C. Pinto ◽  
Camilla C. A. Rodrigues ◽  
...  
Keyword(s):  
Cell Activation ◽  
Mouse Skin ◽  
Skin Inflammation ◽  
Skin Aging ◽  
Ultraviolet B ◽  
Mast Cell Activation ◽  
Tnf Α ◽  
Nrf2 Signaling Pathway ◽  
Total Antioxidant ◽  
And Oxidative Stress

Excessive exposure to UV, especially UVB, is the most important risk factor for skin cancer and premature skin aging. The identification of the specialized pro-resolving lipid mediators (SPMs) challenged the preexisting paradigm of how inflammation ends. Rather than a passive process, the resolution of inflammation relies on the active production of SPMs, such as Lipoxins (Lx), Maresins, protectins, and Resolvins. LXA4 is an SPM that exerts its action through ALX/FPR2 receptor. Stable ALX/FPR2 agonists are required because SPMs can be quickly metabolized within tissues near the site of formation. BML-111 is a commercially available synthetic ALX/FPR2 receptor agonist with analgesic, antioxidant, and anti-inflammatory properties. Based on that, we aimed to determine the effect of BML-111 in a model of UVB-induced skin inflammation in hairless mice. We demonstrated that BML-111 ameliorates the signs of UVB-induced skin inflammation by reducing neutrophil recruitment and mast cell activation. Reduction of these cells by BML-111 led to lower number of sunburn cells formation, decrease in epidermal thickness, collagen degradation, cytokine production (TNF-α, IL-1β, IL-6, TGF, and IL-10), and oxidative stress (observed by an increase in total antioxidant capacity and Nrf2 signaling pathway), indicating that BML-111 might be a promising drug to treat skin disorders.

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