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Unique Herbal-Based Topical Is Comparable to Prescription Retinoid’s Impact on Photoaging and Repair Biomarkers
Abstract
A randomized controlled blinded pilot trial to evaluate the expression of key biomarkers of a topical cream comprising a unique blend of Herbal Extracts (HE) providing anti-inflammatory and stratum corneum repair compared to Tretinoin (Tr) 0.02% cream. Eight peri and post-menopausal women of skin types I-III with moderate to severe photodamage on forearms were evaluated. Two biomarkers for presence of photoaging revealed no statistically significant difference (p < 0.05) between HE and the prescription Tr product . These biomarkers include Fibrillin Ab and procollagen 2. Peroxisome Proliferator Activated Receptor (PPAR) gamma which is a biomarker for epidermal and stratum corneum repair was also tested. Compared to Tr, HE reached a trend toward statistical significance (p = 0.075) superiority in modulating PPAR gamma.
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Background: The world’s population is rapidly aging, and attention to and research on the increase in life expectancy and age-related diseases are needed. This study aimed to review the in vivo studies on the anti-aging effects of herbal medicines. Methods: In vivo studies of single or complex herbal medicines for anti-aging that were published in the last five years were included in this review. The following databases were used: PubMed, Scopus, ScienceDirect, Web of Science and EMBASE. Results: A total of 41 studies were considered eligible for the review. The articles were classified into body organs and functions, experimental country, herbal medicine, extraction method, administration route, dosage, duration, animal model, aging-induced method, sex, number of animals per group, and outcomes and mechanisms A single herbal extract was used in a total of 21 studies including Alpinia oxyphylla Miq., Acanthopanax senticosus and Lyceum barbarum, and a multi-compound herbal prescription was used in a total of 20 studies, including Modified Qiongyu paste, Wuzi Yanzong recipe, etc. Each herbal medicine had anti-aging effects on learning and memory, cognition, emotion, internal organs, gastrointestinal tracts, sexual functions, musculoskeletal function and so on. The common mechanisms of action were antioxidant and anti-inflammatory, and various effects and mechanisms for each organ and function were identified. Conclusions: Herbal medicine exhibited beneficial effects on anti-aging in various parts of the body and its function. Further investigation of the appropriate herbal medicine prescriptions and their components is recommended.
Aging, an inevitable and continuous process in one's lifetime, has all along been a focus of interest, especially for women, yet photoaging treatment to slow the process remains challenging. Recent studies have demonstrated the potency of topical tretinoin in the treatment of photoaging. Tretinoin, a metabolite of retinoids, shows prominent efficacy to regulate proliferation and differentiation of epidermal cells and induce new collagen formation.
Objective:
This review aims to study the current evidence on topical tretinoin for photoaging treatment.
Methods:
A systematic search of the literature was performed from Medline, Cochrane Central, Embase, and PubMed databases for published articles in the past 20 years. Only randomized controlled trials investigating tretinoin for photoaging treatment were included in our review.
Results:
A total of 180 studies were initially examined, of which 7 randomized controlled trials were included in this review. Four studies included only women as their participants, while the rest demonstrated women as their majority subjects. All studies that indicated topical tretinoin were safe and well tolerated in all patients. Topical tretinoin dosage varied from 0.025% to 5% while duration of treatment ranged from 3 months up to 24 months. With regard to efficacy, all studies consistently reported that topical tretinoin was efficacious in improving clinical appearance of photoaging in terms of wrinkling, mottled hyperpigmentation, sallowness, and lentigines as early as 1 month and lasted after 24 months.
Limitations:
Different tretinoin formulas used, different outcome parameters, and limited recent studies on topical tretinoin cause lack of uniformity in the evidences.
Conclusion:
Topical tretinoin is a safe and effective therapeutic modality for long-term treatment of photoaging. Further research is required to compare dose-ranging topical tretinoin to other agents to provide the best treatment strategy for photoaged skin.
The procollagen C-propeptides of the fibrillar collagens play key roles in the intracellular assembly of procollagen molecules from their constituent polypeptides chains, and in the extracellular assembly of collagen molecules into fibrils. Here we review recent advances in understanding the molecular mechanisms controlling C-propeptide trimerization which have revealed the importance of inter-chain disulphide bonding and a small number of charged amino acids in the stability and specificity of different types of chain association. We also show how the crystal structure of the complex between the C-propeptide trimer of procollagen III and the active fragment of procollagen C-proteinase enhancer-1 leads to a detailed model for accelerating release of the C-propeptides from procollagen by bone morphogenetic protein-1 and related proteinases. We then discuss the effects of disease-related missense mutations in the C-propeptides in relation to the sites of these mutations in the three-dimensional structure. While in general there is a good correlation between disease severity and structure-based predictions, there are notable exceptions, suggesting new interactions involving the C-propeptides yet to be characterized. Mutations affecting proteolytic release of the C-propeptides from procollagen are discussed in detail. Finally, the roles of recently discovered interaction partners for the C-propeptides are considered during fibril assembly and cross-linking.
For decades, extrinsic skin aging has been known to result from chronic exposure to solar radiation and, more recently, to tobacco smoke. In this study, we have assessed the influence of air pollution on skin aging in 400 Caucasian women aged 70-80 years. Skin aging was clinically assessed by means of SCINEXA (score of intrinsic and extrinsic skin aging), a validated skin aging score. Traffic-related exposure at the place of residence was determined by traffic particle emissions and by estimation of soot in fine dust. Exposure to background particle concentration was determined by measurements of ambient particles at fixed monitoring sites. The impact of air pollution on skin aging was analyzed by linear and logistic regression and adjusted for potential confounding variables. Air pollution exposure was significantly correlated to extrinsic skin aging signs, in particular to pigment spots and less pronounced to wrinkles. An increase in soot (per 0.5 × 10(-5) per m) and particles from traffic (per 475 kg per year and square km) was associated with 20% more pigment spots on forehead and cheeks. Background particle pollution, which was measured in low residential areas of the cities without busy traffic and therefore is not directly attributable to traffic but rather to other sources of particles, was also positively correlated to pigment spots on face. These results indicate that particle pollution might influence skin aging as well.
Although it is now widely recognized that tobacco smoke has negative effects on the skin, the molecular mechanisms underlying its skin-aging effects remain uncertain. Epidemiological studies indicate that tobacco smoking is a strong independent predictor of facial wrinkle formation and other aspects of premature skin aging. Recent in vivo studies in humans and mice provided the first direct evidence that tobacco smoke causes premature skin aging, and they have begun to reveal the molecular changes in the skin that occur in response to it. Water-soluble tobacco smoke extract, which predominantly produces oxidative stress when applied topically to cultured skin fibroblasts, impairs collagen biosynthesis. Matrix metalloproteinases, which degrade collagen, are induced dose-dependently by tobacco smoke extract as well as by other constituents that trigger the aryl hydrocarbon receptor (AhR), a ligand-dependent transcription factor that mediates the toxicity of several environmental contaminants, including photoproducts in the body generated by UVB radiation. Tobacco smoke also contains many non-water-soluble constituents that activate the AhR pathway. Our most recent studies using hexane-soluble tobacco extract indicate that activation of the AhR pathway may play a role in the premature skin-aging effects of tobacco smoke exposure.Journal of Investigative Dermatology Symposium Proceedings (2009) 14, 53-55; doi:10.1038/jidsymp.2009.13.
For decades it has been appreciated that aging is a consequence of both genetic and environmental influences. Genetic factors are evident, for example, in the > 100-fold variation among species in the rate of aging; and recent studies of fruit flies, worms and even mice have identified specific longevity genes whose modification can greatly alter life-span [27]. Conversely, a role for environmental factors can be deduced both from epidemiological and laboratory-based experimental data. Such influences include ionizing radiation, severe physical and psychological stress, over-eating versus caloric restriction, and in the case of skin ultraviolet (UV) radiation. Among all environmental factors, solar UV radiation is the most important in premature skin aging, a process accordingly also termed photoaging. Over recent years substantial progress has been made in elucidating the underlying molecular mechanisms. From these studies it is now clear that both UVB (290-320 nm) and UVA (320-400 nm) radiation contribute to photoaging. UV-induced alterations at the level of the dermis are best studied and appear to be largely responsible for the phenotype of photoaged skin. It is also generally agreed that UVB acts preferentially on the epidermis where it not only damages DNA in keratinocytes and melanocytes but also causes the production of soluble factors including proteolytic enzymes which then in a second step affect the dermis; in contrast UVA radiation penetrates far more deeply on average and hence exerts direct effects on both the epidermal and the dermal compartment (Fig. 4.1). UVA is also 10-100 times more abundant in sunlight than UVB, depending on the season and time of day. It has therefore been proposed that, although UVA photons are individually far less biologically active than UVB photons, UVA radiation may be at least as important as UVB radiation in the pathogenesis of photoaging [3]. The exact mechanisms by which UV radiation causes premature skin aging is not yet clear, but a number of molecular pathways explaining one or more of the key features of photoaged skin have been described. Some of these models are based on irradiation protocols which use single or few UV exposures, whereas others take into account the fact that photoaging results from chronic UV damage, and as a consequence employ chronic repetitive irradiation protocols. Still others rely on largely theoretical constructs rather than experimental observations.
Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors that modulate the expression of multiple different genes involved in the regulation of lipid, glucose and amino acid metabolism. PPARs and cognate ligands also regulate important cellular functions, including cell proliferation and differentiation, as well as inflammatory responses. This includes a role in mediating skin and pilosebaceous unit homeostasis: PPARs appear to be essential for maintaining skin barrier permeability, inhibit keratinocyte cell growth, promote keratinocyte terminal differentiation and regulate skin inflammation. They also may have protective effects on human hair follicle epithelial stem cells, while defects in PPARγ-mediated signalling may promote the death of these stem cells and thus facilitate the development of cicatricial alopecia (lichen planopilaris). Overall, however, selected PPARγ modulators appear to act as hair growth inhibitors that reduce the proliferation and promote apoptosis of hair matrix keratinocytes. The fact that commonly prescribed PPARγ-modulatory drugs of the thiazolidine-2,4-dione class can exhibit a battery of adverse cutaneous effects underscores the importance of distinguishing beneficial from clinically undesired cutaneous activities of PPARγ ligands and to better understand on the molecular level how PPARγ-regulated cutaneous lipid metabolism and PPARγ-mediated signalling impact on human skin physiology and pathology. Surely, the therapeutic potential that endogenous and exogenous PPARγ modulators may possess in selected skin diseases, ranging from chronic inflammatory hyperproliferative dermatoses like psoriasis and atopic dermatitis, via scarring alopecia and acne can only be harnessed if the complexities of PPARγ signalling in human skin and its appendages are systematically dissected.This article is protected by copyright. All rights reserved.
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