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Abstract The purpose of this research was to identify metabolite change during barley (Hordeum vulgare) germination and reveal active principles for the anti-wrinkle activity. Barley was germinated with deionized water (DW) and mineral-rich water (MRW) for the comparison of the effect of mineral contents on the metabolites changes during germination. The effects of germinated barley extracts (GBEs) on collagen production and collagenase inhibition were evaluated in vitro using human dermal fibroblasts (HDFs). A pronounced anti-wrinkle activity was observed in the test group treated with the MRW-GBEs. In order to find out the active components related to the anti-wrinkle activity, an orthogonal projection to latent structure-discriminant analysis (OPLS-DA) was performed, using the data from secondary metabolites profiling conducted by UPLC–PDA–ESI–MS. The anti-wrinkle activity of MRW-GBEs was revealed to be associated with the increase of oligomeric compounds of procyanidin and prodelphinidin, indicating that it can be used as an active ingredient for anti-wrinkle agents.

Objective: To investigate the anti-senescence effect of 3-bromo-4,5- dihydroxybenzaldehyde (BDB) from Polysiphonia morrowii Harvey in human dermal fibroblasts (HDF). Methods: HDF were subjected to treatment of BDB and then treated with hydrogen peroxide (H2O2) to induce premature senescence. Senescence-associated β-galactosidase (SA-β-gal) activity in HDF was determined using the SA-β-gal staining method. Intracellular reactive oxygen species (ROS) production was measured using the 2’,7’-dichlorodihydrofluorescein diacetate assay. Western blotting assay was performed to assess the level of antioxidant enzyme glutathione peroxidase 1 (GPX1). In addition, intracellular collagen and collagenase contents were analyzed using the respective ELISA kits. Elastase activity in HDF supernatants was measured from p-nitroaniline release and normalized using total protein content. Results: Treatment of HDF with H2O2 increased the activity of SAP-gal, but BDB pre-treatment resulted in the reduction of SA-β- gal activity. Moreover, BDB significantly reduced H2O2-induced intracellular ROS production. BDB also markedly increased the level of GPX1, which was inhibited by 400 µM of H2O2. Furthermore, in in vitro study, BDB significantly increased intracellular collagen content and decreased matrix metalloproteinase-1 and elastase activities in HDF. Conclusions: Our results demonstrate that BDB shows anti- senescence and anti-wrinkle activities in vitro.

The anti-inflammatory activities of the products of supercritical fluid extraction of Litsea japonica fruit (SFELJF) using supercritical carbon dioxide were investigated. The SFELJF extract dose-dependently inhibited the production of inflammatory markers [nitric oxide (NO), inducible nitric oxide synthase (iNOS), prostaglandin E2 (PGE2), and cyclooxygenase-2 (COX-2)] and proinflammatory cytokines [tumour necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6] induced by lipopolysaccharide (LPS) treatment. To further elucidate the mechanisms underlying these inhibitory effects, LPS-induced nuclear factor-κB (NF-κB) activation and mitogen-activated protein kinase (MAPK) phosphorylation were studied. The SFELJF extract inhibited NF-κB (p65 and p50) activation and MAPK [extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38] phosphorylation in a dose-dependent manner. These results suggest that the anti-inflammatory activities of SFELJF extracts are due to proinflammatory cytokines and mediators via suppression of NF-κB activation and MAPK phosphorylation.

The anticancer effects of trans-1,3-diphenyl-2,3-epoxypropan-1-one (DPEP), a chalcone derivative, were investigated in human leukemia HL-60 cells. Treatment of HL-60 cells with various concentration of DPEP resulted in a sequence of events characteristic of apoptosis, including loss of cell viability, morphological changes, and increased sub-G1 DNA content. We demonstrated that DPEP elevates reactive oxygen species (ROS) levels in HL-60 cells, and that the ROS scavenger N-acetylcysteine (NAC) could block DPEP-induced ROS generation and apoptosis. Western blot analysis revealed that DPEP inhibits Bcl-xL expression, leading to caspase-3 activation and poly-ADP-ribose polymerase (PARP) cleavage, thereby inducing apoptosis. However, NAC pre-treatment significantly inhibited the activation of caspase-3 and PARP cleavage and reduced Bcl-xL levels. These findings provide the first evidence that DPEP may inhibit the growth of HL-60 cells and induce apoptosis through a ROS-mediated Bcl-xL pathway. [ABSTRACT FROM AUTHOR]

In this study, the antioxidant properties of 80 % ethanol extracts of 16 species of plants from Jeju Island in Korea were evaluated using various antioxidant assays, including the DPPH (1,1-Diphenyl-2-pricrylhydrazyl) radical scavenging, superoxide scavenging, xanthine oxidase inhibition and hydrogen peroxide scavenging activities. Among the 16 plant extracts tested, CN-13 showed strong antioxidant properties in the DPPH radical scavenging and hydrogen peroxide scavenging tests. The CN-13 ethanol extract was thus selected to be used for further experiments, and was separated into various fractions using four different organic solvents (n-hexane, methylene chloride, ethyl acetate and butanol). The ethyl acetate fraction of CN-13 extract evidenced strong DPPH radical scavenging properties as compared to the other fractions. The ethyl acetate fraction also strongly inhibited DNA-damage induced by hydrogen peroxide-oxidative damage in a mouse lymphoma (L5178Y-R) cell line. Moreover, a correlation between the total phenolic content of the extract, and its antioxidant property was reported. [ABSTRACT FROM AUTHOR]

In this study, we investigated the ability of 6,7-dimethoxy-4-methylcoumarin (DMC) to inhibit lipopolysaccharide (LPS)-induced expression of pro-inflammatory mediators in mouse macrophage (RAW 264.7) cells, and the molecular mechanism through which this inhibition occurred. Our results indicated that DMC downregulated LPS-induced nitric oxide (NO) synthase (iNOS) and cyclooxygenase-2 (COX-2) expression, thereby reducing the production of NO and prostaglandin E2 (PGE2) in LPS-activated RAW 264.7 cells. Furthermore, DMC suppressed LPS-induced production of pro-inflammatory cytokines such as interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α. To elucidate the mechanism underlying the antiinflammatory activity of DMC, we assessed its effects on the mitogen-activated protein kinase (MAPK) pathway and the activity and expression of nuclear transcription factor kappa-B (NF-κB). The experiments demonstrated that DMC inhibited LPS-induced phosphorylation of extracellular signal-regulated kinases (ERKs), c-Jun N-terminal kinase (JNK), and p38. In addition, it attenuated LPS-induced NF-κB activation via the inhibition of I?B-a phosphorylation. Taken together, these data suggest that DMC exerts its anti-inflammatory effects in RAW 264.7 cells through the inhibition of LPS-stimulated NF-κB and MAPK signaling, thereby downregulating the expression of pro-inflammatory mediators. [ABSTRACT FROM AUTHOR]