gallocatechin-3-gallate has been researched along with Disease-Models--Animal* in 2 studies
2 other study(ies) available for gallocatechin-3-gallate and Disease-Models--Animal
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Supplementation of green tea catechins in dentifrices suppresses gingival oxidative stress and periodontal inflammation.
this study examined the effects of a dentifrice containing green tea catechins on gingival oxidative stress and periodontal inflammation using a rat model.. twenty-four male Wister rats were randomly divided into four groups. The first group (Control group) received no treatment for 8 weeks. Periodontal inflammation was induced in the second group for 8 weeks. Periodontal inflammation was induced in the last two groups for 8 weeks and dentifrices with or without green tea catechins were topically applied to the gingival sulcus daily for 4 weeks prior to the end of the experimental period.. rats that had experimental periodontal inflammation showed apical migration of the junctional epithelium, alveolar bone loss and inflammatory cell infiltration in the connective tissue subjacent to the junctional epithelium at 8 weeks, whilst the control group showed no pathologic changes. Topical application of a green tea catechin-containing dentifrice reduced inflammatory cell infiltration in the periodontal lesions to a greater degree than the control dentifrice at 8 weeks. The gingiva in which green tea catechin-containing dentifrice was applied also showed a lower level of expression of hexanoyl-lysine (a marker of lipid peroxidation), nitrotyrosine (a marker of oxidative protein damage), and tumour necrosis factor-α (an indicator of pro-inflammatory cytokines) at 8 weeks compared to gingiva in which the control dentifrice was applied.. adding green tea catechins to a dentifrice may contribute to prevention of periodontal inflammation by decreasing gingival oxidative stress and expression of pro-inflammatory cytokines. Topics: Alveolar Bone Loss; Animals; Antioxidants; Camellia sinensis; Catechin; Connective Tissue; Dentifrices; Disease Models, Animal; Epithelial Attachment; Gingiva; Gingival Recession; Lipid Peroxidation; Lysine; Male; NF-kappa B; Oxidative Stress; Periodontitis; Random Allocation; Rats; Rats, Wistar; Tumor Necrosis Factor-alpha; Tyrosine | 2011 |
Protective effects of EGCg or GCg, a green tea catechin epimer, against postischemic myocardial dysfunction in guinea-pig hearts.
The protective effects of (-)-epigallocatechin-3-gallate (EGCg) or the C-2 epimer, (-)-gallocatechin-3-gallate (GCg), afforded by their antioxidative activity among green tea catechins were investigated in perfused guinea-pig Langendorff hearts subjected to ischemia and reperfusion. The recovery (%) of the left ventricular developed pressure from ischemia by reperfusion was 34.4% in the control, while in the presence of EGCg (3x10(-5) M) or GCg (3x10(-6) M, a more diluted concentration than that of EGCg), it led to a maximal increase of 78.4% or 76.2%, consistent with a significant preservative effect on the tissue level of ATP at the end of ischemia or reperfusion. In the perfused preparation of mitochondria, EGCg (10(-5) M) inhibited mitochondrial Ca(2+) elevation by changes in the Ca(2+) content or the acidification of perfusate, similarly to findings with cyclosporin A, a well known inhibitor of the mitochondrial permeability transition pore. By in vitro electron paramagnetic resonance (EPR), EGCg or GCg was found to directly quench the activity of active oxygen radicals, with the strongest activity in tea catechins. EGCg or GCg decreased the caspase-3 activity induced apoptosis. Therefore, it is concluded that the beneficial effects of EGCg or GCg play an important role in ischemia-reperfusion hearts in close relation with nitric oxide (NO), active oxygen radicals and biological redox systems in mitochondria. Topics: Animals; Antioxidants; Apoptosis; Calcium; Caspase 3; Catechin; Disease Models, Animal; Electron Spin Resonance Spectroscopy; Female; Guinea Pigs; Heart; Heart Ventricles; In Vitro Techniques; Male; Mitochondria; Mitochondrial Membrane Transport Proteins; Mitochondrial Permeability Transition Pore; Myocardial Reperfusion Injury; Myocardium; Perfusion; Reactive Oxygen Species | 2007 |