theasinensin-a has been researched along with Disease-Models--Animal* in 2 studies
2 other study(ies) available for theasinensin-a and Disease-Models--Animal
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Protective effects of theasinensin A against carbon tetrachloride-induced liver injury in mice.
Theasinensins have been identified as a major group of unique catechin dimers mainly found in oolong tea and black tea. Among several types of theasinensins, theasinensin A (TSA), an epigallocatechin gallate (EGCG) dimer with an R-biphenyl bond, is the most abundant theasinensin prevalent in oolong tea. Previous studies have reported that TSA exhibits antioxidative, anti-inflammatory and anti-cancer activities in vitro and in vivo. However, little is known about the hepatoprotective effect of TSA. Thus, the aim of this study was to investigate the inhibitory effect of TSA on carbon tetrachloride (CCl Topics: Animals; Benzopyrans; Camellia sinensis; Carbon Tetrachloride; Disease Models, Animal; Humans; Liver; Liver Cirrhosis; Male; Matrix Metalloproteinase 9; Mice; Phenols; Plant Extracts; Tea; Transforming Growth Factor beta1 | 2017 |
Anti-inflammatory activity and molecular mechanism of Oolong tea theasinensin.
Oolong tea theasinensins are a group of tea polyphenols different from green tea catechins and black tea theaflavins, and they are considered as bioactive compounds in Oolong tea. In the present study, based on the properties of theasinensin and information about inflammatory processes, we investigated the anti-inflammatory activity and molecular mechanisms of theasinensin A (TSA) in both cell and animal models. In the cell model, TSA reduced the levels of pro-inflammatory mediators including inducible nitric oxide synthase (iNOS), nitric oxide (NO), interleukin-12 (IL-12) (p70), tumor necrosis factor alpha (TNF-α), and monocyte chemotactic protein-1 (MCP-1) induced by lipopolysaccharide (LPS). Cellular signaling analysis revealed that TSA downregulated MAPK/ERK kinase (MEK)-extracellular signal-regulated kinase (ERK) signaling. Pull-down assay and affinity data revealed that TSA might directly bind to MEK-ERK for the inhibitory action. In the animal model, TSA suppressed the production of IL-12 (p70), TNF-α, and MCP-1 and attenuated mouse paw edema induced by LPS. Topics: Animals; Anti-Inflammatory Agents; Benzopyrans; Cell Line, Tumor; Chemokine CCL2; Disease Models, Animal; Down-Regulation; Edema; Interleukin-12; Lipopolysaccharides; Macrophages; Male; MAP Kinase Kinase 1; Mice; Mice, Inbred ICR; Nitric Oxide; Nitric Oxide Synthase Type II; Phenols; Plant Preparations; Tea; Tumor Necrosis Factor-alpha | 2014 |