Wheat Ceramide Powder Mitigates Ultraviolet B-Induced Oxidative Stress and Photoaging by Inhibiting Collagen Proteolysis and Promoting Collagen Synthesis in Hairless Mice.

The protective effects of wheat ceramide powder (WC-P) on ultraviolet B (UVB)-induced skin oxidative stress and photoaging in hairless mice were investigated in this study. Moreover, the activities of antioxidant enzymes, inflammation, wrinkle formation-related pathway, and moisturizing capacity were evaluated. Mice were randomly divided into six groups (n=8): normal control (non-UVB irradiation), control (UVB irradiation), L-ascorbic acid [positive control, UVB irradiation with dietary supplementation of L-ascorbic acid at 100 mg/kg/body weight (bw)], WC-P5 (UVB irradiation with dietary supplementation of WC-P at 5 mg/kg/bw), WC-P20 (UVB irradiation with dietary supplementation of WC-P at 20 mg/kg/bw), and WC-P40 (UVB irradiation with dietary supplementation of WC-P at 40 mg/kg/bw). AIN-96G diet and water were supplemented ad libitum, and 100 mL of L-ascorbic acid and WC-P dissolved in water were forcefully administered orally to mice. UVB irradiation resulted in dehydration and wrinkle formation in the dorsal skin of mice. However, WC-P supplementation suppressed. Furthermore, WC-P supplementation enhanced the activites of antioxidant enzymes and expression of transforming growth factor-ß receptor I, procollaten C-endopeptideas enhancer protein, hyaluronan synthase, and ceramide synthase 4 and reduced the activation of the inflammation and the c-Jun N-terminal kinase/c-FOS/c-Jun- mediated matrix metalloproteinase pathways. These findings demonstrate that WC-P can protect the skin from UVB-induced oxidative stress, inflammation, and photoaging by inhibiting collagen proteolysis and promoting collagen synthesis, thereby promoting skin health.

Krill Oil Attenuates Inflammation in Monosodium Iodoacetate-Induced Osteoarthritic Rats, SW982 Synovial Cell Line, and Primary Chondrocytes.

The aim of this study was to investigate the effects of krill oil (FJH-KO) in monoiodoacetate (MIA)-induced osteoarthritis in rat models, and H2O2- or lipopolysaccharide (LPS)-treated primary chondrocytes and the SW982 synovial cell line. We found that 150 mg/kg b.w. FJH-KO supplementation increased running speed, stride, and foot pressure in MIA-induced osteoarthritic rats. In the H2O2-treated SW982 synovial cell line and primary chondrocytes, FJH-KO treatment prevented cell death and suppressed matrix degradation by increasing the levels of anabolic factors of cartilage tissue, including aggrecan, collagen type Ⅰ, collagen type Ⅱ, tissue inhibitors of metalloproteinase (TIMP)-1, and TIMP-3, and decreasing those of catabolic factors of cartilage tissue, including phosphorylation of Smad, MMP-3, and MMP-13. In addition, FJH-KO treatment suppressed the activation of inflammation and apoptosis pathways in the LPS-treated SW982 synovial cell line and primary chondrocytes. We suggest that FJH-KO supplementation may help prevent osteoarthritis progression because of its direct effects on inflammation and apoptosis of chondrocytes.