70 TRENDING TECHNOLOGIES To verify the bitter blend’s ability to
increase intracellular calcium levels, human epidermal keratinocytes were seeded into a 96-well tissue culture plate and grown to confluency in complete media. 0.01%, 0.1%, and 1.0% concentrations of the bitter blend were added to complete media and incubated with keratinocytes. Complete media containing 1mM CaCl2
was utilized as a positive control. 2mM EGTA in the presence of 1mM CaCl2
was utilized as a
negative control. After a 60-minute incubation at 37°C, 50μL of calcium reagent solution was added. The plate was returned to 37°C for 60 minutes followed by 30 minutes at room temperature. Fluorescence measurements were taken
on a Synergy H1 Microplate Reader. The data from this study confirms that the bitter blend increases intracellular calcium levels, an indicator of keratinocyte proliferation, differentiation, and migration, which contributes to the maintenance of skin barrier integrity and homeostasis.
Regulating cellular senescence When our skin’s bitter taste receptors are activated, the body releases calcium and protein essential to the skin barrier and stimulates the synthesis of skin lipids. Utilizing the bitter blend delivers anti-ageing effects through increasing surface metabolism and regulating cellular senescence. Cellular senescence is a state of permanent
cell cycle arrest that accompanies ageing and contributes to a decline in normal skin function and physiology. Senescence is characterized by changes in cellular morphology, metabolism, signalling pathways, and biochemical profiles that manifest as increased collagen breakdown, wrinkles, and thin skin. SA-β-gal is the gold standard biomarker
to identify senescence in vitro as the enzyme β-galactosidase explicitly accumulates in the lysosomes of senescent cells. Accordingly, a cellular ageing model was developed to assess the in vitro effect of the bitter blend to reduce SA-β-gal activity in “aged” keratinocytes. Our data demonstrate ‘young’ keratinocytes
exhibit reduced levels of cellular senescence compared to ‘aged’ keratinocytes, as intended. However, when the ‘aged’ keratinocytes were treated with the bitter blend at 0.01%, 0.1%, and 1.0%, this caused 43%, 47%, and 53% reductions in SA-β-gal activity compared to untreated ‘aged’ keratinocytes, respectively. This key data demonstrates the bitter blend
reduces the cellular senescence in ‘aged’ keratinocytes. Substances that can activate the bitter taste receptor in the skin are beneficial for anti-ageing applications.
Limiting lipid oxidation Our skin is comprised of lipids, and when our lipids experience oxidation, there is cellular damage. To examine the lipid protecting abilities of the bitter blend, we conducted a malondialdehyde (MDA) lipid peroxidation assay. Keratinocytes treated with the bitter blend at 0.01%, 0.1%, and 1.0% demonstrated 1%, 6%,
PERSONAL CARE June 2023 Artichoke
and 29% reductions in MDA concentrations compared to the untreated keratinocytes. The bitter blend’s ability to decrease lipid
peroxidation also represents a decrease in lipid oxidation, resulting in less cellular damage. By preventing this cellular damage, the bitter blend provides a protective effect which may help to mitigate the characteristics of cellular ageing. Cellular ageing can occur from damage can also pose a challenge for repairing damage to the skin’s surface. Our skin has a natural ability to renew as we have discussed, but this self- healing process can be improved by increasing cell migration. To study the ability of skin cells to migrate
and proliferate, we conducted an in vitro scratch assay to compare the wound-healing benefits of the bitter blend. The bitter blend increased cell migration and closed the scratch at a rate comparable to the positive control. The mechanisms of the cells in the in vitro
scratch assay mimic the mechanisms seen in vivo wound healing, so we can be confident that the bitter blend has healing abilities and cell proliferation properties. When the dots are connected, the evidence is clear. This upcycled technology can successfully
activate the skin’s TAS2R bitter taste receptor to effectively provide barrier strengthening, skin homeostasis, and anti-ageing attributes that play a role in achieving a truly modern personal care solution with multitasking benefits.
Conclusion By activating the skin’s bitter taste receptors and encouraging calcium influx, personal care products can now alleviate the previous skepticism around neurocosmetics. This development is not merely fascinating for contemplation in a research lab, but now a readily applicable sensory experience for the skin which combines science, innovation, and efficiency into one solution.
This technological advancement will reframe
the way in which formulators, brands, and consumers perceive neurocosmetic activity and efficacy. The further refinement of activating the skin’s bitter taste receptors will push cosmetic innovation in a refreshing direction. Our skin does more than protect our bones
and organs. It is powerful, and if formulators choose to activate the skin’s bitter receptors in neurocosmetics, the results will be sensational.
PC
References 1. Slominski A, Wortsman J. Neuroendocrinology of the Skin. Endocrine Reviews. Vol. 21, issue 5, 1 October 2000; pages 457–487. https://doi. org/10.1210/edrv.21.5.0410
2. Misery L. Les nerfs à fleur de peau. International Journal of Cosmetic Science. Vol. 24,2 (2002): 111-6. doi:10.1046/j.1467- 2494.2002.00134.x
3. Shaw L, Mansfield C, Colquitt L, Lin C, Ferreira J, Emmetsberger J et al. Personalized expression of bitter “taste” receptors in human skin. Behrens M, editor. PLoS One. 2018 Oct 17; 13(10):e0205322
4. Sang Eun Lee and Seung Hun Lee. Skin Barrier and Calcium. doi: 10.5021/ad.2018.30.3.265
5. Daré RG, Nakamura CV, Ximenes VF, Lautenschlager SOS. Tannic acid, a promising anti-photoaging agent: Evidences of its antioxidant and anti-wrinkle potentials, and its ability to prevent photodamage and MMP-1 expression in L929 fibroblasts exposed to UVB. Free Radic. Biol. Med. doi: 10.1016/j. freeradbiomed.2020.08.019
6. Garrod D. Desmosomes in vivo. Dermatology Research and Practice. Vol. 2010 (2010): 212439. doi:10.1155/2010/212439
7. A. Kowalska U, Kalinowska-Lis. 18β-Glycyrrhetinic acid: its core biological properties and dermatological applications. International Journal of Cosmetic Science.
https://doi.org/10.1111/ics.12548
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