INTRODUCTION
The clinical appearance of aging skin is the result of natural aging superimposed with the effects of the environment or extrinsic aging. While solar radiation remains the most important factor in extrinsic aging, pollution including particulate matter, and ozone also play a role.1 Intrinsically aged skin is characterized by thinning, increasing fragility, paleness, loss of elasticity, and fine wrinkling. In contrast, extrinsically aged skin has course deep wrinkles, mottled pigmentation, brown spots, sallowness, roughness, and dryness. Accordingly, extrinsic aging is often cited as the primary contributor to prematurely aged skin.
While the pathogenesis of intrinsic and extrinsic skin aging has some differences, oxidative stress is common to both. Skin is protected by an array of antioxidants that neutralize reactive oxygen species (ROS) and help prevent oxidative stress.2 Ultraviolet light is the most potent initiator of ROS in skin, however recent data suggests visible and infrared radiation also play a role.3 With aging, antioxidants are diminished, leaving skin more vulnerable to damaging ROS and oxidative stress.4 Accumulation of ROS in the skin can oxidize important biologic molecules such as DNA, proteins, and membrane lipids damaging skin directly. Additionally, in response to oxidative stress, transcription factors in keratinocytes and fibroblasts such as activator protein 1 (AP-1) are upregulated.
AP-1 is responsible for the synthesis of the metalloproteinases enzymes (MMPs) that breakdown collagen.5 AP-1 also inhibits transforming growth factor beta (TGF-β) and reduces collagen production. These effects result in a net loss of dermal collagen, weakening the supporting structure of the skin, and wrinkling. Oxidative stress also upregulates nuclear factor kappa beta (NF-kB) triggering keratinocytes to release a variety of inflammatory mediators such as tumor necrosis factor alpha (TNFα) and interleukin 1 (IL-1).6 This signaling pathway brings activated macrophages, monocytes, and lymphocytes into the skin as well as neutrophils containing collagenases involved in collagen degradation. ROS also contribute to melanogenesis by increasing α-melanocyte stimulating hormone.7
In view of the mechanisms in play that contribute to skin aging, an effective treatment regimen must provide a multimodal approach by combining a variety of active agents to achieve a final positive appearance effect. In this study, we evaluated a treatment regimen with novel ingredients to both protect and repair aging skin. The morning regimen included a serum with a unique combination of antioxidants and peptides to defend against the effects of solar light, pollution, and glycation.8,9,10 This serum also contained encapsulated maslinic acid for skin brightening.11 An elixir containing hydrolyzed pearl, caviar extract, and epidermal growth factor (EGF) was also applied
While the pathogenesis of intrinsic and extrinsic skin aging has some differences, oxidative stress is common to both. Skin is protected by an array of antioxidants that neutralize reactive oxygen species (ROS) and help prevent oxidative stress.2 Ultraviolet light is the most potent initiator of ROS in skin, however recent data suggests visible and infrared radiation also play a role.3 With aging, antioxidants are diminished, leaving skin more vulnerable to damaging ROS and oxidative stress.4 Accumulation of ROS in the skin can oxidize important biologic molecules such as DNA, proteins, and membrane lipids damaging skin directly. Additionally, in response to oxidative stress, transcription factors in keratinocytes and fibroblasts such as activator protein 1 (AP-1) are upregulated.
AP-1 is responsible for the synthesis of the metalloproteinases enzymes (MMPs) that breakdown collagen.5 AP-1 also inhibits transforming growth factor beta (TGF-β) and reduces collagen production. These effects result in a net loss of dermal collagen, weakening the supporting structure of the skin, and wrinkling. Oxidative stress also upregulates nuclear factor kappa beta (NF-kB) triggering keratinocytes to release a variety of inflammatory mediators such as tumor necrosis factor alpha (TNFα) and interleukin 1 (IL-1).6 This signaling pathway brings activated macrophages, monocytes, and lymphocytes into the skin as well as neutrophils containing collagenases involved in collagen degradation. ROS also contribute to melanogenesis by increasing α-melanocyte stimulating hormone.7
In view of the mechanisms in play that contribute to skin aging, an effective treatment regimen must provide a multimodal approach by combining a variety of active agents to achieve a final positive appearance effect. In this study, we evaluated a treatment regimen with novel ingredients to both protect and repair aging skin. The morning regimen included a serum with a unique combination of antioxidants and peptides to defend against the effects of solar light, pollution, and glycation.8,9,10 This serum also contained encapsulated maslinic acid for skin brightening.11 An elixir containing hydrolyzed pearl, caviar extract, and epidermal growth factor (EGF) was also applied
