Dioxinodehydroeckol protects human keratinocyte cells from UVB-induced apoptosis modulated by related genes Bax/Bcl-2 and caspase pathway

Phlorotannins

“…Furthermore, the expression levels of Bax/Bcl-2 and caspase-3, -8, -9, which are the genes associated with apoptosis were investigated when cells were either treated with DHE doses after UVB irradiation or exposed to UVB only. Clear UVB-protective effects were observed in DHE-treated cells (Ryu et al, 2015). In another study, DPHC was used to protect from UVB-induced DNA damages in HaCaT cells (Piao et al, 2015).…”

“…The phlorotannin increased glycerol secretion and reduced glucose consumption level in cells. In addition, effects on PPARg, C/EBPa and differentiationdependent factor 1/sterol regulatory element-binding protein 1c, as well as downstream genes such as fatty acid binding protein-4, fatty acid transport protein-1, fatty acid synthase, leptin and acyl-CoA synthetase 1 were also studied (Kong et al, 2015). In another study by Karadeniz et al (2015), it was reported that phlorotannin suppressed adipogenesis in preadipocytes.…”

Protective effect of gallic acid derivatives from the freshwater green alga Spirogyra sp. against ultraviolet B-induced apoptosis through reactive oxygen species clearance in human keratinocytes and zebrafish

“…Ultraviolet B (UVB), a type of UV in the wavelength ranging from 280 nm to 315 nm, has been studied in the epidermal sun-burn of keratinocytes that are destined to DNA damage and apoptosis after sun exposure. Although humans are exposed to UVA 10 to 100 folds more than UVB, UVB is known to be 1,280 folds more effective at inducing erythema, thus more than 90% of erythema induced by UV irradiation is attributed to UVB (Ryu et al 2015). Furthermore, due to the ozone layer becoming thinner from anthropogenic activities, an excessive amount of UVB in the biosphere is being irradiated .…”

Enhancement of X-ray Induced Apoptosis by Mobile Phone-Like Radio-Frequency Electromagnetic Fields in Mouse Spermatocyte-Derived Cells

“…It has been well documented that the genes encoding Bcl-2 and Bax are involved in the process of apoptosis which is initiated by a death inducing stimulus [22,23,24,25]. Cells showing a higher expression of Bax undergo apoptosis, while those overexpressing Bcl-2 often undergo suppression of apoptosis [26].…”