title: Anti-oxidative and anti-aging activities of 2-O-α-glucopyranosyl-L-ascorbic acid on human dermal fibroblasts.
abstract: A stable ascorbic acid derivative, 2-O-α-glucopyranosyl-l-ascorbic acid (AA-2G), was evaluated and compared with ascorbic acid for its protective effect against cellular damage and senescence induced by hydrogen peroxide (H(2)O(2)). Pretreatment with AA-2G for 72 h promoted the proliferation of normal human dermal fibroblasts (NHDF) and protected against cell damage induced by H(2)O(2). In contrast, ascorbic acid increased the proliferation and protected against cell damage, only when culture medium containing ascorbic acid was replaced every 24 h during the pretreatment period. These results suggest that the effect of AA-2G is longer-lasting compared to that of ascorbic acid. Senescence associated-β-galactosidase (SA-β-gal) activity, a classical biomarker of cellular senescence, was increased in H(2)O(2)-exposed NHDF cells, but pretreatment or posttreatment with ascorbic acid or AA-2G significantly inhibited the increase in SA-β-gal levels. AA-2G was more potent than ascorbic acid in down-regulating SA-β-gal activity. Expression of SIRT1, which has attracted attention as an anti-aging factor in recent years, was significantly decreased in H(2)O(2)-exposed NHDF cells compared to untreated cells. However, pretreatment NHDF cells with AA-2G before H(2)O(2) exposure significantly inhibited this decrease in SIRT1 expression, whereas ascorbic acid had no effect. After H(2)O(2) exposure, the expression levels of p53 and p21 were increased in NHDF cells and pretreatment with AA-2G inhibited this increase. Together, these results suggest that AA-2G protects dermal fibroblasts from oxidative stress and cellular senescence. These characteristics indicate that AA-2G could become a promising material for its anti-aging properties.
authors: Biomedical Institute, Research Center, Hayashibara Biochemical Laboratories, Inc., 675-1 Fujisaki, Naka-Ku, Okayama 702-8006, Japan. ytani@hayashibara.co.jp
authors: Mutsuko
authors: M
authors: Taniguchi
authors: Norie
authors: N
authors: Arai
authors: Keizo
authors: K
authors: Kohno
authors: Shimpei
authors: S
authors: Ushio
authors: Shigeharu
authors: S
authors: Fukuda
mesh_terms: D000975:Antioxidants / Q000494:pharmacology*; D001205:Ascorbic Acid / Q000031:analogs & derivatives* / Q000494:pharmacology; D015415:Biomarkers / Q000378:metabolism; D002453:Cell Cycle / Q000187:drug effects; D016922:Cellular Senescence / Q000187:drug effects*; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000378:metabolism; D004260:DNA Repair / Q000187:drug effects; D005347:Fibroblasts / Q000166:cytology* / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects; D006801:Humans; D006861:Hydrogen Peroxide / Q000494:pharmacology; D056564:Sirtuin 1 / Q000378:metabolism; D012867:Skin / Q000166:cytology*; D014158:Transcription, Genetic / Q000187:drug effects; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
chemical_list: D000975:Antioxidants; D015415:Biomarkers; C493956:CDKN1A protein, human; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016159:Tumor Suppressor Protein p53; C065378:ascorbic acid 2-O-glucoside; D006861:Hydrogen Peroxide; C447939:SIRT1 protein, human; D056564:Sirtuin 1; D001205:Ascorbic Acid