Human skin aging is due to two types of aging processes, “intrinsic” (chronological) aging and “extrinsic” (external factor mediated) aging. While inflammatory events, triggered mainly by sun exposure, but also by pollutants, smoking and stress, are the principle cause of rapid extrinsic aging, inflammation also plays a key role in intrinsic aging. Inflammatory events in the skin lead to a reduction in collagen gene activity but an increase in activity of the genes for matrix metalloproteinases. Inflammation also alters proliferation rates of cells in all skin layers, causes thinning of the epidermis, a flattening of the dermo-epidermal junction, an increase in irregular pigment production, and, finally, an increased incidence of skin cancer. While a large number of inflammatory mediators, including IL-1, TNF-alpha and PGE-2, are responsible for many of these damaging effects, this review will focus primarily on the role of PGE-2 in aging. Levels of this hormone-like mediator increase quickly when skin is exposed to ultraviolet radiation (UVR), causing changes in genes needed for normal skin structure and function. Further, PGE-2 levels in the skin gradually increase with age, regardless of whether or not the skin is protected from UVR, and this smoldering inflammation causes continuous damage to the dermal matrix. Finally, and perhaps most importantly, PGE-2 is strongly linked to skin cancer. This review will focus on: (1) the role of inflammation, and particularly the role of PGE-2, in accelerating skin aging, and (2) current research on natural compounds that inhibit PGE-2 production and how these can be developed into topical products to retard or even reverse the aging process, and to prevent skin cancer.
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