Counteracting the Ramifications of UVB Irradiation and Photoaging with Swietenia macrophylla King Seed

Abstract

In this day and age, the expectation of cosmetic products to effectively slow down skin photoaging is constantly increasing. However, the detrimental effects of UVB on the skin are not easy to tackle as UVB dysregulates a wide range of molecular changes on the cellular level. In our research, irradiated keratinocyte cells not only experienced a compromise in their redox system, but processes from RNA translation to protein synthesis and folding were also affected. Aside from this, proteins involved in various other processes like DNA repair and maintenance, glycolysis, cell growth, proliferation, and migration were affected while the cells approached imminent cell death. Additionally, the collagen degradation pathway was also activated by UVB irradiation through the upregulation of inflammatory and collagen degrading markers. Nevertheless, with the treatment of Swietenia macrophylla (S. macrophylla) seed extract and fractions, the dysregulation of many genes and proteins by UVB was reversed. The reversal effects were particularly promising with the S. macrophylla hexane fraction (SMHF) and S. macrophylla ethyl acetate fraction (SMEAF). SMHF was able to oppose the detrimental effects of UVB in several different processes such as the redox system, DNA repair and maintenance, RNA transcription to translation, protein maintenance and synthesis, cell growth, migration and proliferation, and cell glycolysis, while SMEAF successfully suppressed markers related to skin inflammation, collagen degradation, and cell apoptosis. Thus, in summary, our research not only provided a deeper insight into the molecular changes within irradiated keratinocytes, but also serves as a model platform for future cosmetic research to build upon. Subsequently, both SMHF and SMEAF also displayed potential photoprotective properties that warrant further fractionation and in vivo clinical trials to investigate and obtain potential novel bioactive compounds against photoaging.

The Potential of Sky Fruit as an Anti-Aging and Wound Healing Cosmeceutical Agent

“…Previously, there had been suggestions that the extract of S. macrophylla seeds had photoprotective properties. This can be seen in the research by Mahendra et al [61], where the seed extract displayed the ability to attenuate the damaging effect of UVB on human skin at a molecular level. Hence, although not reaching the critical value of 370 nm, photoprotective bioactive compounds might be present within the S. macrophylla seed extract and its fractions.…”

Cosmeceutical Therapy: Engaging the Repercussions of UVR Photoaging on the Skin’s Circadian Rhythm

“…One well-known role of TIMP3 is the modulation of the inflammatory pathways via TNF-α through TNF-α-converting enzyme (ADAM17) [ 79 ]. As the production of TNF-α under UV exposure induces the release of cytokines, bringing about dermal inflammation and eventually collagen degradation, control of TIMP3 becomes essential in inhibiting photoaging [ 18 , 80 ]. Therefore, the decrease of both AQP3 and TIMP3 by UVB through core clock genes demonstrates the effect UVB has on the skin’s circadian rhythm and its induction of skin photoaging.…”

“…In addition, other studies on proteins, such as Krüppel-like factor (KLF) 9 , peroxiredoxin 2, and sirtuin (SIRT) 3 and 4 , also showed that they all have rhythmic patterns in their expression in the human epidermal keratinocytes [ 86 , 87 , 88 ]. KLF9, a member of the KLF family, was suggested to affect cell proliferation and differentiation, while peroxiredoxins are antioxidant enzymes that are suppressed by UVB radiation [ 18 , 86 , 89 ]. As for SIRTs, they are ADP-ribosyltransferases and NAD (+)-dependent deacetylases that are involved in cell metabolism and epigenetics [ 87 ].…”

“…By mitigating the production of ROS, it could then be expected that melatonin would have an impact on both the skin’s inflammatory and apoptotic pathways [ 111 , 112 ] as the activation of both pathways comes hand-in-hand after the elevation of UVR-induced ROS. Beyond that, with the suppression of cutaneous inflammation, collagen degradation would also be inhibited concomitantly as the production of MMPs is triggered by skin inflammatory agents [ 18 , 113 ]. Overall, the inhibition of this train of events will ultimately lead to delayed premature skin aging which is desired by cosmetic companies.…”

“…In addition, prolonged exposure to sunlight even causes skin cancer as UVB can directly damage DNA by forming cyclobutene pyrimidine dimers (CPD) and pyrimidine-pyrimidone (6-4) photoproducts [ 17 ]. Besides that, the combination of both ultraviolet A (UVA) and UVB, were reported to induce oxidative stress and inflammation of the skin ultimately inciting the formation of irregular pigmentation and degradation of the skin’s extracellular matrixes [ 18 , 19 ].…”