J. Cosmet. Sci., 69, 175–185 (May/June 2018) 175 Understanding Solar Skin Elastosis–Cause and Treatment SABINE PAIN, NICOLAS BERTHÉLÉMY, CORINNE NAUDIN, VÉRONIQUE DEGRAVE, and VALÉRIE ANDRÉ-FREI, BASF Beauty Care Solutions, Lyon 69007, France (S.P., N.B., C.N., V.D., V.A.) Accepted for publication April 4, 2018. Synopsis Photoageing, also called actinic ageing, is the main cause of prematurely aged skin. Our expertise in elastic fi bers has led us to discover a process triggered in response to ultraviolet (UV) light and which upsets the balance of elastin fi bers: there is too much elastin and insuffi cient lysyl oxidase (LOXL1) enzyme to form functional elastic fi bers. This imbalance then leads to an accumulation of nonfunctional elastin, which forms aggregates. In addition to this imbalance, UV rays also induce elafi n synthesis by fi broblasts. Known to be a marker of elastotic aggregates, elafi n crystallizes the elastin fi bers and stimulates the formation of aggregates that cannot be naturally eliminated by the skin. We developed a Hamamelis virginiana leaf extract that was able to restore both the balance between elastin and LOXL1 and to decrease the elafi n synthesis to fi ght and correct the damage. This specifi c Hamamelis virginiana extract increased LOXL1 expression by twofold and decreased elafi n synthesis. As a consequence, elastic fi bers became functional and aggregates of unfunctional fi bers decreased. The specifi c Hamamelis extract activity was confi rmed in vivo with decreasing wrinkles and improving skin fi rmness. INTRODUCTION Cutaneous ageing involves two independent biological processes: chronological (intrin- sic) ageing and extrinsic ageing, the latter of which accelerates normal intrinsic ageing. Tobacco, environmental factors (cold temperature, pollution, and UV rays), mechanical factors, and nutritional factors cause extrinsic ageing (1). However, photoageing (induced by UV radiation) is the main cause of prematurely aged skin, also called actinic ageing. Photoageing principally concerns the exposed parts of the body. The visible effects of actinic ageing depend on the type of individual and are determined by the day-to-day exposure and protection from the sun. During actinic ageing, the epidermis is character- ized by an irregular thickness, either hyperplasic or atrophic (2). As the stratum corneum thickens (keratosic aspect), the superfi cial layers dehydrate. When melanocytes are ex- posed to the sun, their numbers decrease and they are not uniformly spread over the skin, resulting in irregular pigmentary spots. As a consequence, basal cells lose their protection leading to a possible cutaneous carcinoma. Moreover, the dermis is also largely affected by UV radiation. UV-induced ageing is characterized by a signifi cant alteration of conjunc- tive tissue at the collagen and elastic fi ber levels (3). Address all correspondence to Sabine Pain at sabine.pain@basf.com.

JOURNAL OF COSMETIC SCIENCE 176 Solar elastosis is considered to be a sign of chronic sun exposure–related ageing, which is histologically characterized by reduced numbers of dermal collagen fi bers and the accumu- lation of dystrophic elastotic material (4). The elastin fi bers attach themselves forming elastotic aggregates, which form abnormal nonfunctional disintegrated elastic fi bers, leading to a premature ageing phenotype, associated with loss of elasticity, yellow skin, and deeper wrinkles. With ageing, elastic fi bers are abundant, thickened, and disorganized. Elastic fi bers are formed mainly during embryonic development with the deposition of tropoelastin, the soluble precursor of elastin, on a scaffold of fi brillin rich in microfi brils (5–7). The lysyl oxidase (LOXL1) catalyzes the formation of covalent cross-links between some lysine residues of two adjacent tropoelastin molecules, which become insoluble polymer elastin. Mature elastic fi bers consist of an external coat of microfi brils and an amorphous core of cross-linked elastin. These cross-linked amino acids consolidate the polymer, procure its elastic function, and ensure its resistance. The cross-linking step is essential to strengthen the growing elastic fi bers, and this highlights the important role played by LOXL1 in elastogenesis. Moreover, elafi n, also called skin-derived antileukoproteinase, is a serine protease inhibi- tor, mostly produced by epithelial cells. In the skin, keratinocytes are the main source of this molecule. Although elafi n is not detectable in normal skin, it is secreted abundantly in psoriasis and other infl ammatory skin disorders (8). Elafi n acts in various ways on the cutaneous immune homeostasis by not only exerting antiprotease but also by causing immunomodulatory and antiproliferative effects. In the actinic elastosis of sun-damaged skin, fi broblasts express elafi n, (also known as peptidase inhibitor), which binds to elastin. The elafi n–elastin complex hampers the elastolytic regular process, leading to the accu- mulation of abnormal disintegrated elastic fi bers and aggregates (9). The accumulation of elastotic material can be caused by multiple factors, such as a decrease in collagen, an increase in the synthesis of elastin and/or a breakdown of existing and nascent elastic fi bers. We proposed in this study to rebalance the key partners involved in the solar elastosis mecha- nism to improve the level of functional elastic fi bers in the skin exposed to sun radiation. We tested the effect of our new specifi c Hamamelis extract on LOXL1 expression. By increasing LOXL1 expression, our specifi c Hamamelis extract balances elastin/LOXL1 expressions for getting more functional elastin fi bers. The potential of our specifi c Hamamelis extract to counteract the accumulation of abnor- mal elastin fi bers was also evaluated by measuring its capacity to inhibit elafi n expression. Thanks to this clinical study, we have shown that our specifi c Hamamelis extract main- tains youthful skin when exposed to the sun and may be used as a treatment applied at night to relieve the harmful effect of the sun light during the day. METHODS IN VITRO BIOLOGICAL TESTS Active ingredient. In vitro: Hamamelis extract is an extract of leaves of Hamamelis virginiana. Clinical trial. Hamamelis is a formulation containing 1% of water, pentylene glycol, Hamamelis virginiana (witch hazel) leaf extract, xanthan gum, and caprylyl glycol.