Abstract

Soy isoflavones, found in soybean and soybean products, have been reported to possess many physiological activities such as antioxidant activity, inhibition of cancer cell proliferation, reduction of cardiovascular risk, prevention of osteoporosis and alleviation of postmenopausal syndrome. In our previous study, soy isoflavone extract ISO-1 (containing 12 soy isoflavones) from soybean cake was demonstrated to prevent skin damage caused by UVB exposure. In this study, soy isoflavone extract from soybean cake was further purified and evaluated for the protective effects on UVB-induced damage. The results revealed that Fraction 3, which contains the aglycone group (daidzein, genistein and glycitein) and acetylglucoside group (acetyldaidzin, acetylgenistin and acetylglycitin) of soy isoflavones, could inhibit UVB-induced death of human keratinocytes and reduce the level of desquamation, transepidermal water loss (TEWL), erythema and epidermal thickness in mouse skin. Furthermore, topical application of Fraction 3 increased the activity of catalase and suppressed cyclooxygenase-2 (COX-2) and proliferating cell nuclear antigen (PCNA) expression in mice exposed to UVB. In addition, in comparison with ISO-1 and genistein, the Fraction 3 possessed much greater protective effects on both UVB-induced oxidative stress and keratinocyte death than other fractions. Therefore, the soy isoflavone extract Fraction 3 from soybean cake is a desirable anti-photoaging agent for skin care.

Highlights

  • Ultraviolet (UV) radiation, especially UVB (280–320 nm) from sunlight, is one of the major environmental hazards to induce skin damage

  • The result indicated that soy isoflavone extract Fraction 3 from soy cake is non-toxic for human keratinocytes

  • In order to explore the photoprotective effects of Fraction 3 on keratinocytes, cells were treated with Fraction 3 (3, 5, 7.5, 10 μg/mL)

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Summary

Introduction

Ultraviolet (UV) radiation, especially UVB (280–320 nm) from sunlight, is one of the major environmental hazards to induce skin damage. UV exposure could cause edema, erythema, hyperpigmentation, hyperplasia, photoaging, inflammation, DNA damage and mutations in the skin [1,2]. An epidemiologic study reported that long-term exposure to UV radiation raised the risk of skin cancer [3]. P38 were activated by UV exposure, followed by increased expression of cyclooxygenase-2 (COX-2), which contributed to cutaneous inflammation and even carcinogenesis [4]. Reactive oxygen species (ROS), such as H2O2, could be induced by UV exposure and this led to oxidative stress and skin cell damage [5]. Acute and chronic UV exposure caused acute sunburn and skin aging in hairless mice [6]

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