Health-promoting effects of green tea

Abstract

Green tea is manufactured from the leaves of the plant Camellia sinensis Theaceae and has been regarded to possess anti-cancer, anti-obesity, anti-atherosclerotic, anti-diabetic, anti-bacterial, and anti-viral effects. Many of the beneficial effects of green tea are related to the activities of (-)-epigallocatechin gallate (EGCG), a major component of green tea catechins. For about 20 years, we have engaged in studies to reveal the biological activities and action mechanisms of green tea and EGCG. This review summarizes several lines of evidence to indicate the health-promoting properties of green tea mainly based on our own experimental findings.

Figure 1.

Chemical structure of catechins. (−)-Epicatechin, (−)-epigallocatechin, (−)-epicatechin gallate and EGCG are major green tea catechins.

Figure 2.

A model depicting blood-borne metastasis of tumor cells. Cancer metastatic cells invade into the blood flow by degrading the endothelial basement membrane. After adhesion to the blood vessel wall, they extravasate by local degradation to form metastatic tumor colony. Tumor-associated proteinases such as MMPs have critical roles in degradation of the basement membrane containing laminin, collagen IV and fibronectin.

Figure 3.

A model depicting apoptosis through death receptor Fas and the action mechanism of EGCG. CAD, caspase-activated deoxyribonuclease. Binding of EGCG to Fas triggers apoptosis by activating the death receptor signaling.

Figure 4.

The action mechanism of EGCG through inhibition of gene and protein expression of TNF-α. Liver injury induced with galactosamine or ischemia-reperfusion and encephalitis induced with proteolipid protein 139–151 are prevented by EGCG by reducing oxidative stress and/or decreasing TNF-α transcription. Anti-cancer effects of EGCG may include its suppression of TNF-α gene expression. EGCG may also have beneficial effects on TNF-α-associated diseases such as diabetes.

Figure 5.

HNF4α-mediated gene expression of gluconeogenic enzymes. The G6Pase gene promoter contains three HNF4α binding sites and the PEPCK gene promoter has the binding site of its dimer to which several co-factors bind. CRE, cyclic AMP responsive element; DR, direct repeat spaced by one nucleotide; FoxO, forkhead/winged helix box gene group O; GRIP, glucocorticoid receptor-interacting protein; IRS, insulin response sequence; PGC, peroxisome proliferator-activated receptor-γ coactivator.

Figure 6.

Central roles of sterol response element-binding factors (SREBFs) in lipogenesis. Colored thick and thin lines represent the major and minor sites of action for SREBF-1 and SREBF-2, respectively. ACLY, ATP-citrate lyase; ACAC, acetyl CoA carboxylase; FAS, fatty acid synthase; HMGCR, 4-hydroxymethylglutaryl CoA reductase; TCA, citric acid cycle.