Induction of alcohol-metabolizing enzymes and heat shock protein expression by ethanol and modulation by fenugreek seed polyphenols in Chang liver cells.

The present study investigated the effect of fenugreek seed polyphenolic extract (FPEt) on ethanol-induced protein expression in Chang liver cells. Cells were incubated with either 30 mM EtOH alone or together in the presence of FPEt for 24 h. Cells were harvested and assessed for expression of alcohol metabolizing enzymes-alcohol dehydrogenase (ADH(2) isoform), aldehyde dehydrogenase (ALDH(2) isoform), cytochrome P450 (CYP2E1), the electron transport component (cytochrome-c), and the heat shock proteins. The expression of ADH(2), ALDH(2), and CYP2E1 were upregulated, whereas the expression of cytochrome-c was downregulated in the ethanol-treated cells. The expression of cellular heat shock proteins-HSP70, HSC70, HSC92, and mitochondrial protein mtHSP70 were induced in ethanol-treated Chang liver cells. FPEt modulated the protein expression changes induced by ethanol and had no effect when incubated with normal Chang liver cells. FPEt might exert cytoprotective action on ethanol-induced liver cell damage, possibly by enhancing cellular redox status.

In vitro evaluation of the anticancer effect of lactoferrin and tea polyphenol combination on oral carcinoma cells.

We investigated the anticancer effects of green and black tea polyphenols alone and in combination with bovine milk lactoferrin (bLF) on human tongue squamous carcinoma (CAL-27) and normal human gingival fibroblast (HGF) cells. Both green (Polyphenon-E;P-E) and black tea polyphenols (Polyphenon-B;P-B) preferentially inhibit the growth of CAL-27 cells in a dose-dependent manner. Based on the IC(50) values, P-E was found to be more effective than P-B and the combination of P-E and bLF (1:2 ratio) exhibited synergistic inhibition of CAL-27 cells. Analysis of the mechanism revealed nuclear fragmentation and condensation with appearance of the A(o) peak indicative of apoptosis. Furthermore, tea polyphenols transduced the apoptosis signal via generation of reactive oxygen species and decrease in the Bcl-2/Bax ratio thereby inducing mitochondrial permeability transition with consequent activation of caspase-3. Overall, the potency of cytotoxic and apoptosis inducing effects of dietary agents on CAL-27 cells was in the order P-E and bLF combination (1:2 ratio)>P-E>P-B. These results suggest that a "designer" approach may be useful for oral cancer prevention strategies.