Theaflavin Synthesized in a Selective, Domino-Type, One-Pot Enzymatic Biotransformation Method with Camellia sinensis Cell Culture Inhibits Weight Gain and Fat Accumulation to High-Fat Diet-Induced Obese Mice.

The polyphenolic compound theaflavin, which is the main red pigment present in black tea, is reported to elicit various physiological effects. Because of the extremely low concentration of theaflavin present in black tea, its extraction from black tea leaves in quantities sufficient for use in medical studies has been difficult. We have developed a simple, inexpensive, selective, domino-type, one-pot enzymatic biotransformation method for the synthesis of theaflavin that is suitable for use in medical studies. Subsequent administration of this synthetic theaflavin to high-fat diet-induced obese mice inhibited both body weight gain and visceral fat accumulation, with no significant difference in the amount of faeces between the experimental and control mice.

Novel function of rare catechin, epigallocatechin-3-(3''-O-methyl)gallate, against cold injury in primary rat hepatocytes.

Epigallocatechin-3-(3''-O-methyl)gallate (EGCg-3''-OMe) is a rare component in green tea leaf and its bioactivity is hardly known. In this paper, we report that EGCg-3''-OMe has the function for cold preservation of primary rat hepatocytes. Confluent primary cultured hepatocytes were suspended in a storage solution, culture medium or cell banker (CB). EGCg-3''-OMe was tested as a supplement in the storage solution together with a general cryoprotectant, dimethylsulfoxide (DMSO). After 24 h cold preservation of cells at 4 degrees C followed by 1 h rewarming, cell viability and urea-synthesizing activity, one of the most important liver functions, were measured. EGCg-3''-OMe dose-dependently maintained cell viability and this effect was equal to that of a commercial CB at the highest concentration. Cell viability was also maintained after a further 24 h incubation at 37 degrees C of the cold-preserved hepatocytes. Conversely, urea-synthesizing activity was dose-dependently reduced by EGCg-3''-OMe. Cell protection by EGCg-3''-OMe due to the decrease in metabolic activity in cold-preserved cells was suggested. The decreased hepatic function of cells caused by EGCg-3''-OMe was rescued after a further 24 h incubation of cells at 37 degrees C.

Suppression of cytotoxin-induced cell death in isolated hepatocytes by tea catechins.

To elucidate the hepatoprotective effects of green tea catechins, the following experiments were conducted utilizing (-)-epigallocatechin-3-gallate (EGCG), the major component of green tea catechin, together with other catechins. The protective effects of catechins against hepatotoxins, bromobenzene or rubratoxin B, were examined in primary cultures of rat hepatocytes. Bromobenzene and rubratoxin B are known to induce necrosis and apoptosis of cells, respectively. After 24-h treatment with toxin, EGCG and (-)-epigallocatechin-3-(3"-O-methyl)gallate (EGCg-3"-OMe) suppressed the bromobenzene-induced morphological change and dose-dependently prevented bromobenzene-induced cell death. Both catechins also prevented apoptotic cell death caused by rubratoxin B. In rubratoxin B-treated cells, both catechins were found to suppress the activation of caspase-3 by rubratoxin B. The results in the present study suggest that EGCG and EGCg-3"-OMe are potent hepatoprotective agents. This report is the first to show that catechins suppress cytotoxin-induced cell death.