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Altay Benetti, A.; Tarbox, T.; Benetti, C. Mechanisms of Therapeutics and Cosmetic Agents against Aging. Encyclopedia. Available online: https://encyclopedia.pub/entry/42991 (accessed on 29 September 2024).
Altay Benetti A, Tarbox T, Benetti C. Mechanisms of Therapeutics and Cosmetic Agents against Aging. Encyclopedia. Available at: https://encyclopedia.pub/entry/42991. Accessed September 29, 2024.
Altay Benetti, Ayça, Tamara Tarbox, Camillo Benetti. "Mechanisms of Therapeutics and Cosmetic Agents against Aging" Encyclopedia, https://encyclopedia.pub/entry/42991 (accessed September 29, 2024).
Altay Benetti, A., Tarbox, T., & Benetti, C. (2023, April 12). Mechanisms of Therapeutics and Cosmetic Agents against Aging. In Encyclopedia. https://encyclopedia.pub/entry/42991
Altay Benetti, Ayça, et al. "Mechanisms of Therapeutics and Cosmetic Agents against Aging." Encyclopedia. Web. 12 April, 2023.
Mechanisms of Therapeutics and Cosmetic Agents against Aging
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This entry is adapted from the peer-reviewed paper 10.3390/cosmetics10020054

Skin is the protective physical barrier that protects our body against harm from the hazardous effects of ultraviolet (UV) radiation and the infiltration of pathogens, as well as the dehydration process. Skin aging can be divided into two types of processes: intrinsic, or chronological aging, and extrinsic aging.  The agents presented here were chosen as representatives of some of the most commonly used types of anti-aging therapeutics.

skin aging cosmetics matrikines

1. Synthetic and Plant-Derived Products

1.1. Synthetic Products

Doxycycline is a tetracycline antibiotic and an innate matrix metalloproteinase (MMP) inhibitor used in the treatment of periodontal disease [1]. It has been reported to be able to inhibit MMP-2 and MMP-1 expression in vivo [2][3]. The key role of the doxycycline-mediated inhibition of MMPs was discussed in the study by Chiarelli et al. Their study focused on the treatment of hypermobile Ehlers–Danlos syndrome (hEDS), which is associated with extracellular matrix (ECM) organization as it is generally characterized by abnormalities in the ECM. Based on the findings from human studies, it was determined that doxycycline, which is generally used against hEDS, restores the organization of the ECM and reverts the dysfunction of dermal fibroblasts [4].
Diclofenac is a non-steroidal anti-inflammatory drug (NSAID) that likely reduces prostaglandin E2 by way of cyclooxygenase inhibition. Diclofenac has been shown to localize in the epidermis synergistically with hyaluronic acid (HA), but not with other glycosaminoglycans, pharmaceutical gelling agents, or in buffer [5]. At 3% in a 2.5% HA topical gel, diclofenac has been shown in randomized control trials to effectively reduce and clear actinic keratosis lesions that commonly present on the face and hands from excessive ultraviolet (UV) exposure [5].

1.2. Vitamins

Many vitamins are important because of their antioxidant capabilities in human systems. They can decrease ROS in human cells, leading to the production of low-activity molecules. Moreover, they help aging skin cells reduce their oxidative damage in such a manner that the generation of key components of skin cells increases. Further studies have revealed new natural products for anti-aging and additional antioxidant effects of vitamins C, D, A, B12, B3, and E, as well as lipoic acid and coenzyme Q10.
Vitamin D is the most commonly used natural product amongst anti-aging therapeutic agents. Even though UV radiation initiates its biosynthesis, findings show that vitamin D can protect DNA from damage caused by UV radiation, thereby protecting the skin [6]. Vitamin C, or L-ascorbic acid, is an antioxidant that is essential for collagen synthesis, and indirectly scavenges superoxide by formation of an intermediate radical [7][8]. In clinical studies, a 3% oil-in-water (O/W) emulsion was shown to reduce facial wrinkles and a 5% cream was shown to facilitate elastic tissue repair involving dermal papillae [9][10]. Vitamin E, or d-α-tocopherol, is an antioxidant that has been shown to inhibit molecularly induced oxidative changes including AP-1 binding in UV-irradiated keratinocytes in a dose-dependent manner [11]. Vitamin E upregulates antioxidant enzymes, scavenges superoxide, and inhibits lipid oxidation [8]. Most research involves mixtures of vitamin E with other antioxidants, such as vitamin C and coenzyme Q10 [12][13].
The regulation mechanism of MMPs is studied during the formulation development of natural compounds, such as folic acid and vitamin B12, which are expected to work as AhR antagonists. According to the study by Kim et al. [14], to impede the formation of wrinkles and DNA damage mediated by MAPK pathways and associated with the induction of UV irradiation, the AhR antagonists should be used via transdermal delivery against skin aging.

1.3. Endogenous Compounds

Ubiquinone or coenzyme Q10 (CoQ10) has a similar structure to vitamin K, but is synthesized throughout the body, is fat-soluble, and functions as both a pro- and antioxidant [13]. The actual mechanism of CoQ10 against skin aging is to maintain the skin cell organization by impeding the generation of ROS, which is known to regulate the production of MMPs via the activation of the MAPK pathway. Thus, some formulation studies focused on the reduction in MMP-1 expression after UVA exposure in order to demonstrate the efficacy of topical administration of CoQ10. Oral supplementation of CoQ10 when using its water-soluble formulation with improved bioavailability was shown to reduce wrinkles and increase smoothness [15][16].
Retinoids belong to the vitamin A family and are commonly used against skin aging as natural compounds. They are commonly known as retinoic acid, which has the same molecular and functional properties as all related retinol compounds, and prevents the skin from deformation by regulating MMPs [17].
Tretinoin, or all-trans-retinoic acid, is a vitamin A metabolite that can modulate cellular programming in the skin through retinoic acid receptors (RARs) and retinoid X receptors (RXRs) [18], such as by inhibiting the UV-induced activation of NF-κB and AP-1 [19]. The use of retinoids results in epidermal thickening, SC compaction, and synthesis of glycosaminoglycans, thereby decreasing the signs of photoaging in vivo, but with the unfortunate side effects of a burning sensation and dryness [19].
Hyaluronic acid (HA), a major polyanionic glycosaminoglycan found in the ECM, is composed of N-acetyl-d-glucosamine and β-glucuronic acid, and has been shown to uniquely enhance SC penetration and localization of certain therapeutic agents to the epidermis, including clindamycin, cyclosporine, and select NSAIDs [5]. The exact mechanism is unknown, but may involve HA receptors within the skin and the facilitation of drug retention within the HA-hydrated epidermal layers [5][20].

1.4. Carotenoids

Astaxanthin, a natural pigment synthesized by yeasts, bacteria, plants, and microalgae such as Haematococcus pluvialis, has been shown in a number of studies to significantly improve clinical signs of photoaged skin related to wrinkles, elasticity, and moisture when administered topically and/or orally [21]. With a greater antioxidant capacity than β-carotene, astaxanthin has been shown to block NF-κB activation and inhibit MMP-3 and MMP-1 expression in vitro, leading to reduced inflammation and increased collagen content [22]. Lutein, another xanthophyll carotenoid capable of filtering blue light, has been demonstrated to be protective against skin damage caused by UV radiation, likely through its role as an antioxidant [23].

1.5. Polyphenols

Resveratrol is an all-natural stilbene that can be extracted from grapes and is thought to reduce signs of aging processes in skin through the inhibition of apoptotic occurrences and mitochondrial dysfunctions [24]. Resveratrol has been shown to modulate inflammatory cytokines such as IL-6, IL-8, and tumor necrosis factor-alpha (TNF-α) in human keratinocytes, thanks to the production of phosphorylated EGFR (epidermal growth factor receptor) [25].
Epigallocatechin gallate (EGCG), a tannin from green tea extract, is an antioxidant that has been shown to reduce oxidative stress and inhibit NF-κB in vitro for protection against UV radiation [25]. Although claimed to provide anti-aging benefits for the skin, minimal human clinical data have been published, including one study that evaluated UV-induced damage for a broad-spectrum sunscreen with and without EGCG. While sunscreen alone decreased the amount of MMP-1 detected in the skin, the addition of EGCG resulted in a significantly greater reduction in MMP-1 [26][27].
Apigenin, a flavone found in many plants, is reported to have anti-inflammatory and antioxidant effects in vitro [28]. When administered to mouse skin inflamed by UVB light, apigenin-containing ethosomes were shown to reduce cyclooxygenase-2, an important enzyme in the synthesis of prostaglandins [29]. The function of apigenin was recently demonstrated in the study by Che-Hwon Park et al., which focused on the mechanism of skin disease and the evaluation of apigenin-mediated amelioration. This study showed that the production of nitric oxide (NO), the expression of cytokines (IL-1, IL-4, IL-5, IL-6, and COX-2), and the phosphorylation of MAPKs were significantly inhibited by apigenin; therefore, it has good potential as a therapeutic agent for autoimmune diseases such as psoriasis [30][31].
Baicalein and baicalin, flavones found in Scutellaria baicalensis, are reported to have a good range for inhibiting the mechanism of not only cancer, but also UVA exposure, ROS, and bacterial infections via LI-promoted Fenton chemistry [31]. The extract of S. baicalensis was shown to diminish the excessive release of oxidative stress and to neutralize the production of ROS. Thus, the main mechanism of baicalin has been related to its anti-inflammatory function owing to the inhibition of NF-κB, COX-1, and iNOS [31][32].

2. Peptides, Cell-Derived Products, and Biologics

2.1. Peptides, Proteins, and Cell Culture-Derived Extracts

Carnosine, an endogenous dipeptide (β-alanyl-l-histidine) that is synthesized in muscle and brain cells, has been credited with cell-regenerating and lifespan-extending properties in cultured human fibroblasts, but the evidence beyond preclinical studies is limited [33]. Data suggest that carnosine administration can suppress the growth-inhibitory cytokine TGF-β, which inhibits telomerase, as well as increase circulating IGF-1, which is associated with reduced wrinkles [34][35].
Recently, Aldag, Teixeira, and Leventhal summarized clinical evidence for selected peptides and proteins used cosmetically for aging, including matrikines, matrikine-like peptides, growth factors, cytokines, and protein extracts, complementing the previous summary by Gorouhi and Maibach [36][37]. Clinical investigations have been performed to evaluate the efficacy of some of these therapeutic agents (Table 1), which supports the label claims on related marketed products.
As shown in Table 1, many of these products contain matrikines or matrikine-like peptides. As matrikines are peptide fragments released through the proteolysis of ECM components that can trigger the synthesis activity of collagens, elastin, and glycosaminoglycans, they have proven useful in anti-aging treatments [38]. These peptides have beneficial growth factor-like activities, but are much smaller and simpler to utilize for formulation purposes [39]. Minor modifications to the peptide structures, such as by adding palmitoyl to KTTKS or octanoyl to carnosine, have led to significant improvements in skin permeation, and thus, to efficacy [38][40].
Table 1. Products containing matrikines and matrikine-like peptides.
Brand Ingredient(s) Origin Cosm. Use Mechanism Delivery System Ref.
Iamin GHK-Cu or copper tripeptide-1 fragment of the α2-chain of collagen I anti-aging enhances Cu2+ uptake, TIMP-1, TIMP-2, and MMP-2; promotes degradation of collagen aggregates; promotes collagen, elastin, proteoglycan, and glycosaminoglycan production; anti-inflammatory and antioxidant hydrogel
alternative: microneedles		 [37][41][42][43]
Matrixyl pal-KTTKS, palmitoyl pentapeptide-4, palmitoyl pentapeptide-3, or palmitoyl oligopeptide procollagen I-derived pentamer (KTTKS) with palmitoyl added to improve permeability anti-aging promotes the production of fibronectin, elastin, glycosaminoglycans, and collagen types I, III and VI; stabilizes mRNAs that upregulate TGF-β O/W emulsion moisturizer [37][40][44]
Preregen soybean protein, glycine soy protein, and amino acids soybean seed anti-aging inhibits proteinase formation and increases number of dermal papillae O/W emulsion in Tegocare-45 base [37][45]
Keramino 25 keratin protein and amino acids human hair and sheep wool anti-aging moisturizer improves elasticity and hydration of the skin and hair multilamellar vesicle liposomes, 0.9% NaCl [37][46]
Citrix CRS cell rejuvenation system (L-ascorbic acid, TGF-β1, and Cimicifuga) recombinant TGF-β1, stem cell extract from Cimicifuga racemosa anti-aging profibrotic cytokine modulates angiogenesis, cellular migration and proliferation, neocollagenesis, and degradation of matrix proteins liposome cream in silicone base [37][47]
Processed skin cell proteins (PSP) PSP bio-restorative skin cream (mixture of cytokines and growth factors) human fibroblast cell culture lysate anti-aging growth factors promote angiogenesis and cytokines modulate inflammation cream [36][48][49]
Nouricel-MD TNS tissue nutrient solution recovery complex (VEGF, PDGF-A, G-CSF, HGF, IL-6, IL-8, and TGF-β1) human neonatal foreskin fibroblast culture anti-aging growth factors promote angiogenesis, and cytokines modulate inflammation and enhance ECM component deposition oil-free gel [36][37][48]
ReGenica, MRCx MRCx (VEGF, IL-8, and keratinocyte growth factor, but no TGF-β) Cytokines and growth factors from conditioned medium of fibroblasts anti-aging moisturizer growth factors promote angiogenesis and cytokines modulate inflammation cream [36][50]
Micro-protein complex (MPC) GEGK, pal-GHK, and N-octanoyl-carnosine synthetic anti-wrinkle increases ECM collagen, hyaluronan, and fibronectin cream [36][39][51]
Decorinyl tripeptide-10 citrulline, or Lys-α-Asp-Ile-citrulline synthetic decorin-like tetrapeptide anti-aging regulates collagen fibrillogenesis, and improves uniformity of and influences diameter and position of collagen fibers liposomal cream [37][52]
Progeline trifluoroacetyl-tripeptide-2 or trifluoroacetyl-Val-Tyr-Val synthetic anti-wrinkle inhibits MMP and decreases the synthesis of
progerin, and improves the relation of collagens via the production of
proteoglycan		 cream [53]
SYN®-AKE tripeptide-3 or
dipeptide diamino
butyroyl
benzylamide
diacetate		 Synthetic tripeptide mimicking Waglerin-1 from
snake venom		 anti-wrinkle formulated for the treatment of neuromuscular activity; inhibits the muscular activity associated with repeated movement at the neuromuscular junction Hydrogel = glycerin-based aqueous solution [53][54][55]

2.2. Biologics and DNA Repair

Botulinum toxin (BTX) is generated in the anaerobic spore of the Clostridium bacteria. This toxin is a complex mixture of botulinum neurotoxin and several non-toxic proteins [56]. Botulinum toxin has eight distinct antigenic profiles (A–G), but their presence depends on the different strains of Clostridium botulinum. The human nervous system can develop botulism if it comes in contact with the A, B, C, E, F, and G strains, but it is unaffected by the D strain [57]. BTX is synthesized as a single-chain polypeptide that becomes a double chain with a disulfide bridge thanks to the action of proteases (a process known as activation) [56][57].
SP1, SP2, and SP3, which are high-affinity monoclonal antibodies targeting mouse MMP-1A, MMP-2, and MMP-3, respectively, were made using protein engineering from scFv fragments identified using phage-display library screening experiments [58]. There was no cross-reactivity, low nanomolar binding affinity (KD 6 nM), or low or undetectable expression of the MMP-1A antigen in healthy tissue, indicating the excellent potential of the SP1 antibody in disease-targeting applications, which could translate to advancements in skin aging and possibly new effective and non-toxic MMP inhibitor treatments [59].
T4 endonuclease V, or T4N5, is a bacteriophage-derived DNA repair enzyme that has been shown to reduce cyclobutane pyrimidine dimers (CPDs) and MMP-1 activation caused by UV irradiation in keratinocytes [7]. When administered topically after UV exposure in a randomized clinical study as pH-sensitive liposomes in a hydrogel lotion, the removal of UV-induced CPDs was accelerated compared to the placebo [60].

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Subjects: Dermatology
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Ayça Altay Benetti
,
Tamara Tarbox
,
Camillo Benetti
View Times: 379
Revisions: 2 times (View History)
Update Date: 13 Apr 2023
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