We investigated whether standardized edible bird’s nest extract (BNE-PK) can prevent ultraviolet B (UVB) irradiation-mediated oxidative stress and photoaging in the skin using in vitro and in vivo models. BNE-PK increased skin hydration by hyaluronic acid synthesis and activation of ceramide synthase in UVB-irradiated hairless mice and HaCaT cells. Furthermore, BNE-PK suppressed melanogenesis by down-regulation of the cAMP/PKA/CREB/MITF/TRP-1/TRP-2/tyrosinase pathway in UVB-irradiated hairless mice and 3-isobutyl-1-methylxanthine (IBMX)-treated B16F10 cells. In UVB-irradiated hairless mice, BNE-PK attenuated the wrinkle formation-related JNK/c-FOS/c-Jun/MMP pathway and activated the TGF-βRI/SMAD3/pro-collagen type I pathway during UVB-mediated oxidative stress. Based on these findings, our data suggest that BNE-PK may potentially be used for the development of effective natural anti-photoaging functional foods for skin health.

Consistent ultraviolet B (UVB) radiation exposure results in dry skin, wrinkles, and melanogenesis. In this study, we investigated whether fish collagen peptide (Naticol Ⓡ ) could inhibit photoaging and oxidative stress in skin exposed to UVB using cell and animal models. We measured the skin hydration, histological observations, antioxidant activities, moisturizing-related factors, collagen synthesis-related factors, and melanogenesis-related factors in skin cells and animal skin using enzyme-linked immunosorbent assay, real-time polymerase chain reaction, and Western blot assay. NaticolⓇ collagen improved skin moisturization via hyaluronic acid and ceramide synthesis-related factors in HaCaT cells and SHK-I hairless mice that were exposed to UVB. In addition, Naticol Ⓡ collagen inhibited wrinkle formation in Hs27 cells and SHK-I hairless mice exposed to UVB and restrained melanogenesis in 3-isobutyl-1-methylxanthine-induced B16F10 cells and UVB-irradiated SHK-I hairless mice. On the basis of these findings, we propose that ingestion of Naticol Ⓡ collagen might be valuable for preventing skin photoaging.

This study aimed to investigate whether low molecular fish collagen peptide (FC) from Oreochromis niloticus had protective effects on skin of photoaging mimic models. We observed that FC supplementation improved antioxidant enzymes activities and regulated the pro-inflammatory cytokines [e.g., tumor necrosis factor-, interleukin (IL)-1, and IL-6] by reducing the protein expressions of pro-inflammatory factors IB, p65, and cyclooxygenase-2 in ultraviolet-B (UV-B) irradiated in vitro and in vivo. Furthermore, FC increased hyaluronic acid, sphingomyelin, and skin hydration by regulating the mRNA expression of hyaluronic acid synthases 1∼3, serine palmitoyltransferase 1, delta 4-desaturase, sphingolipid 1, and protein expressions of ceramide synthase 4, matrix metalloproteinase (MMP)-1, -2, and -9. In UV-B irradiated in vitro and in vivo, FC down-regulated the protein expression of the c-Jun N-terminal kinase, c-Fos, c-Jun, and MMP pathways and up-regulated that of the transforming growth factor- receptor I, collagen type I, procollagen type I, and small mothers against decapentaplegic homolog pathways. Our results suggest that FC can be effective against UV-B induced skin photoaging by improving skin dryness and wrinkle formation through antioxidant and anti-inflammatory properties.

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Background: Obesity, abnormal fat accumulation in the adipose tissue, has become a serious global public health problem as it increases an individual’s risk of developing various diseases. Objective: This study sought to determine whether the extract from sunflower seed (SUNCA) prevents the development of obesity in high-fat diet (HFD)-induced obese mice. Design: C57BL/6J mice were fed with AIN93G normal diet (Normal diet), 60% HFD, HFD containing Catechin 100 mg/kg body weight (b.w.) (Catechin), HFD containing SUNCA 25 mg/kg b.w. (SUNCA 25), HFD containing SUNCA 50 mg/kg b.w. (SUNCA 50), or HFD containing SUNCA 100 mg/kg b.w. (SUNCA 100) for 15 weeks. Results: Body weight gain, food efficiency rate, adipose tissue weight, adipose tissue mass, size of adipocytes, and serum levels of triglyceride, total cholesterol, very low-density lipoprotein/low-density lipoprotein (VLDL/LDL)-cholesterol, aspartate aminotransferase, and alanine aminotransferase were significantly decreased by SUNCA supplementation in HFD-fed mice. Furthermore, SUNCA supplementation decreased the expression of proteins related to the adipogenesis and lipogenesis pathways and increased the expression of proteins related to the lipolysis and thermogenesis pathways in the adipose tissues of HFD-induced obese mice. Conclusions: Altogether, SUNCA might prevent obesity by suppressing the adipogenesis/lipogenesis pathway and stimulating the lipolysis/thermogenesis pathway in HFD-induced obese mice.