Characterizing the Chemoprevention Potential of Amenity Grass Phenolic Extracts In Vitro and the Corresponding Nutraceutical Targets within HepG2 Carcinoma Cells
نویسنده
چکیده
Adviser: Roch Gaussoin This research has revealed significant chemopreventive potential belonging to the planet's most renewable and abundant plant source: amenity grasses. The characterization results from Chapter 1 demonstrated the potential chemoprevention attributes of supina bluegrass and bermudagrass crude extracts linked to the extensive phenolic acid profiles of these amenity grasses. In contrast to cereals, amenity grass phenolic extracts (AGPE) offer appreciable amounts of unbound/free ferulic acid that would be available for rapid in vivo absorption. The literature has shown ferulic acid to be a highly available and health benefitting phenolic compound. Chapter 1 in vitro studies demonstrated AGPE-induced antiproliferation and apoptotic induction capacities in HepG2 and Caco-2 carcinoma cell lines. The in vitro chemopreventive influences were shown to be dependent upon AGPE species, extract fraction, dose, and cell line. As with most natural systems, a significant gap in knowledge exists as to how such health promoting components modulate metabolism to maintain health. Thus, the objective of Chapter 2 was to monitor the metabolic alterations attributed to supina bluegrass and bermudagrass phenolic treatments in human hepatocellular liver carcinoma cells, HepG2, using Fourier Transform mid infrared (FT-mIR) spectroscopy. The FT-mIR ! metabolomic method was used to assess temporal changes in the biochemical fingerprint of treated and untreated HepG2 cells compared to resveratrol positive control treatments. The results from this study illustrate amenity grass nutraceutical targets within the HepG2 metabolme compared to the documented biochemical influences of resveratrol. As an outcome to this study, the impacts of nutraceutical stimuli on the biochemical fingerprint were further elucidated by analyzing the ability of phenolics to downregulate the oxidative nature of cancer.
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