Importance: These data may be useful for developing guidelines for clinicians and the general population related to the reversal of photoaging effects on the aging face damaged by solar radiation.

Objective: To investigate antiaging effects of 4 commercially available topical agents on the dorsal skin in photoaged hairless mice.

Design And Setting: Animal study at an academic medical center. Animals comprised 56 female Skh-1 hairless mice (6-8 weeks old). Skin samples were collected from nonirradiated intact mice (control), mice irradiated with UV-B for 8 weeks, mice irradiated with UV-B and then exposed to a topical cosmeceutical applied for 5 weeks, and UV-B-irradiated mice not exposed to cosmeceuticals and retained for 5 weeks until the end of the experiment.

Intervention: The mice were exposed to UV-B light 3 times a week for 2 months, followed by topical application of a peptide, antioxidant, estrogen, and retinoic acid agent for 5 weeks.

Main Outcomes And Measures: Surface features such as wrinkling were analyzed from replicas along with histomorphometric determination of epidermal thickness, sebocyte counts, and immunohistochemical study of proliferating cell nuclear antigen (PCNA).

Results: Exposure to UV-B induced significant wrinkle formation after 13 weeks, which was attenuated with treatments with a peptide cream, antioxidant mixture, and estrogen cream (mean [SD] Rz values: control [C], 60.7 [19.0]; irradiated [RAD], 51.8 [15.9] [P < .001]; irradiated-long [RAD-long], 86.0 [28.3] [P = .01]; antioxidant [AO], 45.2 [13.2]; peptide, 63.4 [18.8], estrogen, 64.6 [21.2]; retinoic acid [RA], 73.9 [28.5]; RAD-long vs C [P = .01], vs RAD [P < .001], vs estrogen [P = .04], vs peptide [P = .02], vs AO [P<.001], vs RA [P = .25]. There was a trend of reversal of irradiation-induced augmentation of epidermal thickness in animals treated with the peptide and AO (mean [SD] epidermal width: C, 21.0 [2.2] μm; RAD, 41.3 [7.0] μm [P < .001]; RAD-long, 39.1 [11.0] μm [P = .006]; AO, 37.3 [14] μm [P < .001]; peptide, 33.9 [3.8] μm [P = .01]; estrogen, 59.2 [9.2] μm [P = .003]; RA, 52.4 [8.7] μm [P < .001]). Retinoic acid augmented epidermal width and sebocyte counts (mean [SD] sebocyte data [number per gland]: C, 9.4 [2.0]; RAD, 11.69 [1.5] [P < .001]; RAD-long, 6.5 [1.3] [P = .73]; peptide, 7.2 [1.7] [P = .03]; estrogen, 4.1 [0.9] [P < .001]; AO, 7.2 [1.7] [P = .06]; RA, 11.0 [1.4] [P = .01]). Estrogen cream was effective in restoring surface features but enhanced thickness of epidermis in irradiated specimens. All groups had a higher PCNA index score except for peptide treatment, which brought it down to the control level (mean [SD] PCNA index values: C, 17.3 [1.5]; RAD, 32.4 [6.8] [P < .001]; RAD-long, 34.0 [6.1] [P < .001]; AO, 62.1 [3.5] [P = .01]; peptide, 20.1 [6.3] [P < .001]; estrogen, 56.8 [10.0] [P < .001]; RA, 35.2 [10.2] [P < .001]).

Conclusions And Relevance: Of the 4 cosmeceuticals tested within this experimental period, peptide cream and antioxidant mixture were the most effective overall in reversing photoaging effects; retinoic acid was the least effective of these topical agents.

Level Of Evidence: NA.

Download full-text PDF

Source
http://dx.doi.org/10.1001/jamafacial.2013.2582DOI Listing

Publication Analysis

Top Keywords

uv-b-irradiated mice
8
mice irradiated
8
irradiated uv-b
8
mice exposed
8
mice
7
weeks
5
cosmeceutical skin
4
skin surface
4
surface profiles
4
profiles epidermis
4

Similar Publications

Skin homeostasis is predominantly compromised by exposure to UV-B irradiation, leading to several physiopathological processes at cellular and tissue levels that deteriorate skin function and integrity. The current study investigated the photo-protective role of seabuckthorn fruit pulp (SBT) extract against UV-B-induced damage in primary human skin fibroblasts (HDFs) and Balb/C mice skin. We subjected HDFs and Balb/C mice to UV-B irradiation and measured multiple cellular damage indicators.

View Article and Find Full Text PDF
Article Synopsis
  • MC1R is a receptor in melanocytes that regulates melanin production via α-MSH, while TLR4, found in various cell types, activates immune responses and also enhances melanin production through the NF-κB pathway.
  • Benzimidazole-2-butanol (BI2B) has been identified as an inhibitor of the LPS/TLR4 pathway and shows potential in reducing excess pigmentation by targeting the α-MSH-induced melanogenic process.
  • In tests involving UV-B-irradiated mouse skin and activated melanocyte cultures, BI2B effectively decreased levels of melanogenic markers and disrupted key signaling pathways linked to pigmentation, highlighting its role in managing hyperpigmentation.
View Article and Find Full Text PDF

UV-B radiation induces sunburn, and neutrophils are pivotal in this inflammation. In this study, we examined the potential involvement of neutrophil extracellular traps (NETs) in ultraviolet B (UVB)-induced skin inflammation, correlating the skin inflammation-mitigating effects of Hochu-ekki-to on UV-B irradiation and NETs. To elucidate NET distribution in the dorsal skin, male ICR mice, exposed to UVB irradiation, were immunohistologically analyzed to detect citrullinated histone H3 (citH3) and peptidylarginine deiminase 4 (PAD4).

View Article and Find Full Text PDF

The cAMP response element-binding protein (CREB) and CREB-regulated transcription coactivators (CRTCs) cooperate in the transcriptional activation of microphthalmia-associated transcription factor subtype M (MITF-M) that is a master regulator in the biogenesis, pigmentation and transfer of melanosomes at epidermal melanocytes. Here, we propose the targeting of phosphorylation circuits on CREB and CRTCs in the expression of MITF-M as the rationale to prevent skin hyperpigmentation by elucidating the inhibitory activity and mechanism of yakuchinone A (Yaku A) on facultative melanogenesis. We employed human epidermal melanocyte cell, mouse skin, and mouse melanoma cell, and applied Western blotting, reverse transcription-polymerase chain reaction, immunoprecipitation and confocal microscopy to conduct this study.

View Article and Find Full Text PDF

Background: DNA is the main target for UV-B-irradiation-induced skin photodamage and accounts for 90 % of all the non-melanoma skin cancers.

Purpose: In this study, we explored the mechanistic basis of photoprotective effect of Trigonelline, a naturally occurring alkaloid from the Trigonella foenum-graecum, against UV-B-induced oxidative DNA Damage Response using Primary Human Dermal Fibroblasts (HDFs) and BALB/C mice as models of skin photodamage.

Methods: Primary HDFs were subjected to UV-B exposure (10 mJ/cm) with or without TG for 24 h.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!