Abstract
Loliolide is a monoterpenoid hydroxylactone present in freshwater algae that has anti-inflammatory and antiaging activity; however, its effects on ultraviolet-damaged skin have yet to be elucidated. This study investigated the antiapoptosis and wound-healing effects of loliolide using HaCaT cells (a human keratinocyte cell line). Loliolide inhibited the expression of reactive oxygen species (ROS) induced by ultraviolet radiation as well as wrinkle formation-related matrix metalloproteinase genes and increased the expression of the damage repair-related gene SIRT1. The apoptosis signaling pathway was confirmed by Western blot analysis, which showed that loliolide was able to reduce the expression of caspases 3, 8, and 9, which are related to ROS-induced apoptosis. In addition, Western blotting, reverse-transcription polymerase chain reaction (PCR), and real-time PCR analyses showed that loliolide enhanced the expression of the epidermal growth factor receptor signaling pathway (PI3K, AKT) and migration factors, such as K6, K16, and K17; keratinocyte growth factor; and inflammatory cytokines, such as interleukin (IL)-1, IL-17, and IL-22 expressed during the cellular scratching process, suggesting a putative wound-healing ability. Because of the antiapoptosis and antiscratching effects on skin of both loliolide and loliolide-rich Prasiola japonica ethanol extract, we consider the former to be an important compound used in the cosmeceutical industry.
Highlights
Skin is a self-renewing organ that defends the body against external threats such as heat, infections, mechanical or chemical insults, and ultraviolet (UV) radiation [1,2]
The apoptosis signaling pathway mechanism is known to be controlled as caspases 3, 8, and 9 [11]
Jr.eMcool.vSecir.e2d019th, 1e7,d0o00w0 n-regulated level of cell viability of UV-irradiated HaCaT cells, impl3yionf g17a putative photoprotective effect against cell death caused by UVB-induced oxidative stress (Figure 2b)
Summary
Skin is a self-renewing organ that defends the body against external threats such as heat, infections, mechanical or chemical insults, and ultraviolet (UV) radiation [1,2]. Skin exposure to UV can induce erythema, DNA damage, formation of reactive oxygen species (ROS), and skin inflammation and wrinkling, among other outcomes [4,5]. ROS generation has been proven to be related to the skin’s collagen degradation through the activation of matrix metalloproteinases (MMPs) [6], which leads to both skin sagging and wrinkling. UV exposu including cell detachment, ceclalnsihnrdiunckeatghe,ecxhpreosmsioantinof cthoencdyecnlosoaxtyiognen, aasned-2 D(CNOAX-2f)raggenme,ewnthaitcihocnau[1se0s].skin inflammation, The apoptosis signaling pathwweallyasmtoecthaendioswmnrisegkunlaotiwonn otfoSbiret-1c,oantgreonleleidnvboylvepdrointeUolVy-tiincdeuncezdymDNesA damage repair, ce such as caspases 3, 8, and 9 [s1u1r]v. The apoptosis signaling pathway mechanism is known to be controlled as caspases 3, 8, and 9 [11] Since both skin wrinkling and apoptosis can by proteolytic be induced by enzym ROS, on.
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