0115 966 7955 Today's Opening Times 10:00 - 20:00 (GMT)
Place an Order
Instant price

Struggling with your work?

Get it right the first time & learn smarter today

Place an Order
Banner ad for Viper plagiarism checker

UV-Protective Effects of Soy Extracts in Cosmeceuticals

Disclaimer: This work has been submitted by a student. This is not an example of the work written by our professional academic writers. You can view samples of our professional work here.

Any opinions, findings, conclusions or recommendations expressed in this material are those of the authors and do not necessarily reflect the views of UK Essays.

Published: Fri, 06 Apr 2018

UV-Protective effects of soy extracts in cosmeceuticals

1.0 Introduction

Current changes in climate may have bothered many population of human around the globe. Thinning of ozone layer in the atmosphere aggravates the UV transmittance from the sun to the earth, which potentiate injurious skin effects when exposed to UV radiation [6]. The rising clinical cases of photo-induced skin problems covers from skin tanning until life-threatening skin cancer. Ultraviolet (UV) radiation, particularly UVB (280-320 nm) from sunlight is one of the main environmental hazards to cause skin damage [1]. Such exposure may lead to edema, erythema, hyperpigmentation, hyperplasia, photoaging, immunosuppression, sunburn, inflammation and mutations of skin [1,6]. In photoaging, it is marked by the presence of fine and coarse wrinkles, textural changes and loss of skin elasticity. One of the therapies which has been used, be it mythological or based on factual findings, is soy extracts.

Soy isoflavones are composed of glucosides (daidzin, genistin and glycitin) and aglycone (daidzein, genistein and glycitein) which play a role in health benefits of soy. These two different isoforms exist naturally in the isoflavones [1]. Though both protein and isoflavone components contained in the soy may have variety in their health benefits, the most beneficial extracts of the soy are exhibited by isoflavones [4]. It has been demonstrated to possess the physiological effects of antioxidants, anti-inflammatory activities [1] and health-benefit in cardiovascular disease [4]. In regard to the UVB-induced skin damage, soy isoflavones prevent keratinocyte death. By suppressing UVB-induced intracellular H2O2 release, it also reduces oxidative stress in the body [1]. Plus, topical application of daidzein (an aglycone) effectively reduces the cancer occurrence induced by chronic solar UV radiation and it provides UV-protective antioxidant effects [2]. Application of genistein topically inhibits both initiation and promotion of skin tumour [5]. In short, soy extracts give a wealthy health advantages in terms of its UV-protective benefits onto the skin. The following review regards the action of soy isoflavone in exhibiting the UV-protective effects.

2.0 Mechanism of action

Several different possible mechanism of action appeared to be responsible for the biological health of body, particularly on the skin. Majority of in vitro research to date has narrowed down the potential benefits of soy isoflavones into the effects of skin aging through anti-inflammatory effect of isoflavones and the effects of photocarcinogenesis through inhibition of cell proliferative activities.

2.1 Genistein inhibits COX-2 activities

Irradiation of human skin fibroblasts by UVB lead to expression of Cyclooxygenase 2 (COX-2) level and Growth Arrest and DNA-damage inducible (Gadd45) gene, of which both are involved in inflammation process and DNA repair, respectively [2]. Cellular responses, such as aging and carcinogenesis are caused by COX-2 expression induced by UV radiation [11]. COX-2 is an enzyme responsible for inflammation and pain when there is an extrinsic stimulus acts against the body. Addition to non-steroidal anti-inflammatory drugs (NSAIDs), isoflavones also showed inhibitory effects on the COX-2 expression. In inflammation process, expression of UVB-induced COX-2 in human epidermal cell cultures is inhibited by genistein. Due to this anti-inflammatory profile, it supresses the prostaglandin E2 synthesis as stimulated by UVB [13]. Prostaglandin is a vital mediator to cause inflammation effect.

Gadd45 gene is a regulator for cell cycle and a DNA repair gene. It functions as a stress sensor and subjected to strees-signaling responses, be it physiological or environmental stressors. Stressful conditions, such as ionizing radiation induce Gadd45 gene expression [7]. Consequently, this leads to cell cycle arrest, cell survival and senescence, DNA repair or apoptosis. The mechanism of Gadd45 protein coordinates the responses of cells towards the stressors is unclear [7].

2.2 Glucoside combination proves more beneficial

In a study conducted by Iovine et.al, treatment of UVB-induced DNA damage by using genistin or daidzin before irradiation did not show significant prevention of the damage. In other way around, treatment using glucoside combination of genistein and daidzin proved most effective protection against UVB-induced DNA damage [2]. This is also supported by another report by Iovine et al which showed that the combination of isoflavones (in this case is genistein and daidzein) proved more effectively in preventing DNA damage caused by UVB [7].

2.3 Inhibition of tyrosine protein kinases and phosphorylation of EGF-receptor

Phosphorylation of the epidermal growth factor receptor (EGFR) occurs as physiologic doses of UVB radiation are exposed to human keratinocytes [15]. Usage of isoflavone such as genistein blocks the action of tyrosine kinases (TPK) and phosphorylation of EGF-R, thus hindering the intracellular signalling pathway in human keratinocytes [9]. It is a potent tyrosine kinase inhibitor and may inhibit cell proliferation and differentiation [4]. Irradiation by UVB substantially initiates the phosphorylation of EGF-R and mitogen-activate protein kinase (MAPK) [10]. H202 plays a significant role in this process. UVB exposure to human keratinocytes generates H2O2, which mediates EGF-R phosphorylation [15]. This phosphorylation process can be inhibited by dose-dependently incubate or treat with genistein.

TPK-dependent EGF-R phosphorylation and MAPK activation are related to the initiation of transcription factors (promoting activities); release of inflammatory mediators, for instance, prostaglandins; and stimulation of cell proliferation. UVB-activated EGF-R can also lead to an increase in the thickness of the epidermis [10]. Hence, the inhibitory effects of genistein to the UVB-induced EGF-R phosphorylation and MAPK activation suggests its potential anti-promotional effects [9]. However, the tyrosine kinase effects brought by genistein have been postulated to be irrelevant to its potential health advantages due to doses required to produce such effects [14].

2.4 Blocks pyrimidine dimer formation

UVB irradiation can initiate oxidative DNA damage represented by 8-hydroxy-deoxyguanosine (8-0HdG) and photodynamically-damaged DNA, as in pyrimidine dimer (PD) formation. 8-OHdG is a hallmark of carcinogenesis and aging and PD is a precursor of signature mutation of P53 genes. Formation PD and 8-OHdG in skin can be substantially promoted by UVB irradiation. Wei et al reported that in their study, UVB-exposed skins of euthanized mice were harvested for level of PD and 8-OHdG after the treatment with genistein. It was found that genistein significantly inhibited both PD and 8-OHdG formation in a dose-dependent regime [9]. In study conducted by Moore et al, pre-treatment of skin sample with dose-dependent regime of genistein prior to UV exposure can demonstrate a reduction in PD formation. An observable result can be seen in UV-induced DNA damage secondary to UV exposure in the absence of genistein after the treatment with genistein, whereby the damage has been significantly reduced in the skin sample [8].

Pharmacokinetics

the isoflavone aglycone forms have poor solubility in water and oil; thus, a special galenic mixture is necessary to introduce these isoflavone preparations into cosmetic formulations [2].

Structure/medchem

Genistein (4’,5,7-trigydroxyisoflavone) [7]


To export a reference to this article please select a referencing stye below:

Reference Copied to Clipboard.
Reference Copied to Clipboard.
Reference Copied to Clipboard.
Reference Copied to Clipboard.
Reference Copied to Clipboard.
Reference Copied to Clipboard.
Reference Copied to Clipboard.

Request Removal

If you are the original writer of this essay and no longer wish to have the essay published on the UK Essays website then please click on the link below to request removal:


More from UK Essays