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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: 9,10-Dimethyl-1,2-benzanthracene, Animals, Apoptosis, Cell Nucleus, Cell Proliferation, Cell Transformation, Neoplastic, Cyclin-Dependent Kinase Inhibitor p21, Enzyme Activation, Epidermis, Female, Flavonoids, Inflammation Mediators, MAP Kinase Signaling System, Mice, Ornithine Decarboxylase, Phenols, Polymers, Polyphenols, Precancerous Conditions, Protein Kinase Inhibitors, Proto-Oncogene Proteins c-akt, Skin Neoplasms, Tea, Tetradecanoylphorbol Acetate, Transcription Factors, Tumor Suppressor Protein p53.
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Do polymeric black tea polyphenols inhibit mouse skin chemical carcinogenesis by decreasing cell proliferation? Context: The aim of this study was to investigate the antitumour promoting effects and possible mechanisms of action of the most abundant polymeric black tea polyphenols (PBPs 1-5) or thearubigins, in vivo. Effect of PBP pre-treatments on 12-O-tetradecanoylphorbol-13-acetate (TPA) promoted skin papillomas was studied in 7,12-dimethylbenz(a)anthracene initiated mice over 40 weeks. Cell proliferation and apoptosis, in epidermis of the skin, were measured using appropriate immunohistochemical staining. Mitogen-activated protein kinase signalling studies were conducted with Western blot analysis at 10, 20, 30 and 40 weeks of promotion. Pre-treatments with PBP fractions differentially altered latency, multiplicity and incidence of skin papillomas as compared to TPA treatments thereby exhibiting antipromoting effects. Most PBP fractions decreased TPA-induced cell proliferation by decreasing activation of signalling kinases (c-Jun N-terminal protein kinase, extracellular signal-regulated protein kinase, p38 protein kinase and Akt), transcription factors (activator protein-1 and nuclear factor kappa B) and inflammatory protein (cyclooxygenase 2). TPA-induced epidermal cell apoptosis was also decreased by pre-treatment with most PBP fractions. Higher levels of p53 and p21 in skin cells pre-treated with PBP fractions followed by TPA treatment as compared to only TPA-treated animals suggested possible activation of a cell cycle checkpoint.
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PBP-2 was observed to be the most potent polymeric polyphenol fraction and PBP-4 and PBP-5 showed only marginal activity, whereas PBP-1 and PBP-3 displayed intermediate efficacies. In conclusion, the protective effects of PBP fractions could be attributed to inhibition of TPA-induced cellular proliferation. Final Decision: yes