UV radiation-induced skin aging in hairless mice is effectively prevented by oral intake of sea buckthorn (Hippophae rhamnoides L.) fruit blend for 6 weeks through MMP suppression and increase of SOD activity

Abstract

Oxidative stress and oxidative photodamage induced by UV radiation can cause serious skin damage that is characterized by wrinkling, roughness, laxity and pigmentation. The effects of a sea buckthorn (Hippophae rhamnoides L.) fruit blend (SFB) containing sea buckthorn fruit extract, blueberry extract and collagen on UV-induced skin aging were examined by treating hairless mice for 6 weeks with UV irradiation and SFB administered orally. The effects of SFB were measured in the skin of these mice by phenotypical and histological analysis and western blotting. According to wrinkle formation analysis, the oral intake of SFB induced a decrease in wrinkle formation in the damaged skin of UV-irradiated mice. The thickness of the epidermis and dermis in the vitamin extracts (Vit)- and SFB-treated group was lower than that in the vehicle-treated group, but the group treated with SFB50 was the most effective group. The mice treated with the Vit- or SFB solution maintained a normal moisture content through the inhibition of transdermal water loss (TEWL) and an increase in skin moisture content. Furthermore, the levels of matrix metalloproteinase (MMP) and collagen protein expression were assessed in five groups to examine the mechanisms underlying the effects of SFB oral intake. The application of SFB induced a decrease in MMP-1 and -9 expression to the levels observed in the vehicle-treated group, but MMP-9 expression showed a much larger decrease than MMP-1. Furthermore, the expression of collagen-1 in the skin corresponded to MMP expression except for the SFB30-treated group, whereas the superoxide dismutase (SOD) activity was increased dramatically in the SFB50-treated group. These results suggest that SFB has potential as a protective and therapeutic drug candidate against skin aging that functions by regulating the moisture content, MMP expression levels and SOD activity.

Hippophae rhamnoides L. 沙棘 (Shaji, Common Sea-buckthorn)

“…Isorhamnetin inhibited hydrogen peroxide-induced apoptoic damage in H9c2 cardiomycotes by suppressing the production of reactive oxygen species and activating ERK and p53 [22], in addition to the inhibition of the overproduction of ox-LDL-induced reactive oxygen species in endothelial cell Eahy926 [23]. Sea buckthorn fruit feeding alleviated oxidative stressinduced skin damage in mice exposed to UV irradiation [24]. Sea buckthorn seed oil displayed hepatic protection in a carbon chloride induced mice model by improving their antioxidant defense system and suppressing lipid oxidation [25].…”

“…A high antioxidant fruit blend containing sea buckthorn and blueberry fed to hairless mice suffering from UV irradiation resulted in a reduction of wrinkle formation and transdermal moisture loss. Sea buckthorn administration reduced the overly expressed matrix metalloproteinase (MMP) MMP-1 and MMP-9 induced by irradiation, and improved SOD avidity dramatically [24]. The dermal healing and anti-apoptotic effects of sea buckthorn fruit and oil for acute and chronic skin problems have been extensively investigated in various animal models with wounds, burns, and scalds [19,28].…”

Sea Buckthorn Oil—A Valuable Source for Cosmeceuticals

“…Most commonly, it is added to anti-aging and anti-wrinkle cosmetics due to its firming and tonifying properties for aging skin [5]. Hwang et al (2012) suggested a sea buckthorn fruit blend against skin aging, because it functions by regulating moisture content, matrix metalloproteinase expression levels, and superoxide dismutase (SOD) activity [56]. SB oil alleviates dry, irritated, rough, flaking, and itchy skin [57].…”

DCP-LA Exerts an Antiaging Action on the Skin

“…UV exposure enhances ROS/RNS production [4,5,6], and the free radicals cause skin damage including apoptosis by interacting with DNAs, RNAs, and proteins [7]. Several lines of evidence have pointed to the implication of mitogen-activated protein kinase, aryl hydrocarbon receptor, transcription factors, such as nuclear factor-κB and nuclear factor erythroid 2-related factor 2, or matrix metalloproteinase in the degradation of dermal connective tissue following oxidative stress-induced skin damage [8,9,10,11,12,13,14,15]. …”