Potential anti‐ageing effect of chondroitin sulphate through skin regeneration

Abstract

Objective Skin ageing is inevitably exposed through its typical features such as wrinkles and sagging. Therefore, skin anti‐ageing is a major issue in cosmetic research to prevent and improve ageing symptoms using effective ingredients. Chondroitin sulphate (CS), a type of glycosaminoglycan, is an important structural component of the extracellular matrix (ECM) and is involved in various biological processes, such as cell proliferation, differentiation and migration. Here, we aimed to investigate the effects of CS on skin regeneration and examine its efficacy as a potential safe and effective skin anti‐ageing ingredient. Methods We investigated the effects of CS on cell proliferation in normal human keratinocytes and fibroblasts. Then, cell migration, ECM synthesis and related signalling pathways were examined in fibroblasts through gene and protein expression analysis. Finally, the effect on skin wound healing and regeneration was validated using a full‐thickness skin wound model and an aged skin model. Results Chondroitin sulphate treatment increased the proliferation of keratinocytes and fibroblasts. It also stimulated the migration and synthesis of ECM components of fibroblasts. Further analysis revealed that CS induced the expression of type I procollagen by activating the extracellular signal‐regulated kinase pathway. Using a full‐thickness skin wound model and an aged skin model, we confirmed that CS treatment promoted skin wound healing and regeneration. Conclusion Together, our results indicated that CS has the potential to facilitate skin regeneration, implying that CS could be clinically applied to improve skin ageing.

Alpha-Tocopherol Protects Human Dermal Fibroblasts by Modulating Nitric Oxide Release, Mitochondrial Function, Redox Status, and Inflammation

“…We focused our attention on fibroblasts since these are the main cell components involved in skin repair and aging processes. While in physiologic conditions, they are almost resting, in the presence of any skin injury, they show abnormalities in the metabolism and proliferation, which can be at the basis of aging skin structure changes [30,31]. Even more relevant is the involvement of the senescent fibroblasts not only in the early stages of skin carcinogenesis [32] but also in cancer cell migration and metastasis, both in melanoma [33] and in NMSC [34].…”

Transcriptomic and epigenetic assessment of ageing male skin identifies disruption of Ca2+ homeostasis; exacerbated by smoking and UV exposure

“…Creating age group categories and stratifying by sex reduced variance, increased sample sizes, and created data sets following a negative binomial distribution. The GTEx repository contained both fibroblast and skin samples, detailed age, sex, UV-exposure status and smoking status of participants, and covered a greater age range which made it highly advantageous, given the impact that these factors can have on skin ageing 1,3,4,6,7 . Clustering identified that fibroblasts were transcriptomically distinct from skin samples, so skin and fibroblasts were analysed Smoking and UV-exposure; known to accelerate visible signs of skin ageing were used to generate additional stratification's, hone in on ageing signatures, and investigate the impacts of these environmental factors.…”

“…Consequently significant Gene Ontology categories represent alterations in keratinisation, keratinocyte differentiation, protein targeting to the membrane and ER, cell surface receptor signalling, biological and cell adhesion All of these changes are seen in middle aged UV-exposed male skin, indicating disruption of the membrane barrier and disruption to the calcium gradient. Waterproofing, and cornification steps are dependent on transglutaminase activity, which is regulated by intracellular Ca 2+ , which is in turn regulated by extracellular Ca 2+ and thus disruption of the calcium gradient, disrupts cornification 2 , which could explain age related increases in trans-epidermal water loss 6 and observed dermal thinning 3,7,9 . In old age (> 65) cornification is the most significantly reduced process, consequently genes involved in keratinisation (KRTs, KRTAPs, SPRRs) and collagen (COL11A1, COL3A1, COL4A4, COL8A1) generation are decreased, leading to the identification of skin development functional categories 9.…”

“…Intrinsic ageing encompasses the spontaneous appearance of fine wrinkles and thinning of the epidermis with advancing age 1, 2 ; influenced by ethnicity, anatomical variation, and hormones 3 , which differ by age and sex [4][5][6] . Extrinsic ageing encompasses accelerated changes in skin structure and function, evidenced by deep wrinkles, skin laxity, and hyperpigmentation, which can be brought about by chronic UV-exposure which alters the concentrations and localisation of adhesion proteins 1,[3][4][5] , pollutant exposure, excessive alcohol consumption, and smoking 1,3,4,[6][7][8] . The rate of ageing can be affected by alterations in the vascular / glandular network, and hydration 1,7 .…”

Primary Ciliogenesis by 2-Isopropylmalic Acid Prevents PM2.5-Induced Inflammatory Response and MMP-1 Activation in Human Dermal Fibroblasts and a 3-D-Skin Model

“…A full-thickness human 3-D-skin model was reconstructed through slight modification of our previously described protocols [37,38]. Briefly, dermal mixture was prepared by mixing Type-I collagen (3 mg/mL, Nitta gelatin, Osaka, Japan), reconstruction buffer (Nitta gelatin), DE concentrated culture solution (Nitta gelatin), fibrinogen (10 mg/mL, Sigma-Aldrich.…”