Protective Effect of Amaranthus cruentus L. Seed Oil on UVA-Radiation-Induced Apoptosis in Human Skin Fibroblasts

Abstract

Since the exposure of fibroblasts to prolonged UVA radiation induces oxidative stress and apoptosis, there is a need for effective skin protection compounds with cytoprotective and antioxidant properties. One of their sources is Amaranthus cruentus L. seed oil (AmO), which is rich in unsaturated fatty acids, squalene, vitamin E derivatives and phytosterols. The aim of this study was to evaluate whether AmO evokes a protective effect on the apoptosis induced by UVA radiation in human skin fibroblasts. UVA radiation at an applied dose of 10 J/cm2 caused a significant reduction in the survival of human skin fibroblasts and directed them into the apoptosis pathway. Increased expression of p53, caspase-3, caspase-9 and PARP proteins in UVA-treated fibroblasts suggests the intrinsic mechanism of apoptosis. Application of the oil at 0.1% and 0.15% concentrations to UVA-treated cells decreased the expression of these proteins, which was accompanied by increased cell survival. Similarly, the UVA-dependent decrease in the expression of p-Akt and mTOR proteins was restored under the effect of the studied oil. The molecular mechanism of this phenomenon was related to the stimulation of antioxidant processes through the activation of Nrf2. This suggests that AmO stimulated the antioxidant system in fibroblasts, preventing the effects of UVA-induced oxidative stress, which may lead to pharmaceutical and cosmetological applications as a sun-protective substance.

Amaranthus cruentus L. Seed Oil Counteracts UVA-Radiation-Induced Inhibition of Collagen Biosynthesis and Wound Healing in Human Skin Fibroblasts

“…We found that AmO at 0.05%, 0.1%, and 0.15% concentrations evoked a protective effect on decreased viability of fibroblast exposure to UVA irradiation [13]. Exposure to UVA radiation at a dosage of 10 J/cm 2 resulted in the down-regulation of p-AKT and mTOR expression, alongside the upregulation of p53, caspase-3, caspase-9, and PARP expression.…”

“…The underlying molecular mechanism of this phenomenon is linked to the stimulation of antioxidant processes through the activation of Nrf2. This implies that AmO stimulates the antioxidant system in fibroblast cells, counteracting the effects of UVA-induced oxidative stress [13]. These data led us to evaluate the effect of AmO on collagen metabolism in fibroblasts exposed to UVA radiation.…”

“…Seed oil derived from Amaranthus cruentus L. (AmO) is considered a promising source of bioactive compounds counteracting UVA-induced skin damage [13]. The grains of Amaranthus cruentus L. cultivated for their seeds exhibit a greater lipid content (7.2%) compared to traditional cereal plants.…”

Molecular hydrogen (H2) – therapeutic properties for the skin and methods of application

“…Promieniowanie UV jest głównym czynnikiem stymulującym produkcję reaktywnych form tlenu w skórze, głównie w zakresie UVA (320-400 nm) [15], z pewnym nakładaniem się na zakres UVB. Po ekspozycji na UV obserwuje się wykrywalne poziomy nadtlenku wodoru (H 2 O 2 ) i rodników hydroksylowych (•OH).…”

“…Promieniowanie UVA dodatkowo zmniejsza ekspresję kinaz p-AKT i mTOR, jednocześnie zwiększając ekspresję białek p53, kaspazy-3, kaspazy-9 i polimeraz poli (ADP-rybozy) inaczej PARP. To prowadzi do znacznego zmniejszenia przeżywalności fibroblastów skóry ludzkiej, indukując ich apoptozę [15].…”