**8. Herbal**

gallocatechin (9–12%), epicatechin gallate (9–12%) and epicatechin (5–7%) [42]. The catechin content of green tea depends on several factors including how the leaves are processed be‐ fore drying, preparation of the infusion and decaffeination, as well as the form in which it is distributed in the market (instant preparations, iced and ready-to-drink teas have been shown to contain fewer catechins) [43]. When tea leaves are rolled or broken during indus‐ try manufacture, catechins come in contact with polyphenol oxidase, resulting in their oxi‐ dation and the formation of flavanol dimers and polymers known as theaflavins and

Tea leaves destined to become black tea are rolled and allowed to ferment, resulting in rela‐ tively high concentrations of theaflavins and thearubigins and relatively low concentrations of catechins. Consequently, green tea contains relatively high concentrations of catechins and low concentrations of theaflavins and thearubigins. It is important to underline that black tea administration to LDL receptor-deficient mice did not affect aortic fatty streak le‐ sion area, although fatty streak lesion areas in the same animal model supplemented with anti-oxidants, such as vitamin C, vitamin E and β-carotene, were 60% smaller than those of control animals [44,45]. On the other hand, green tea catechins have been shown to inhibit formation of ox-LDL, may decrease linoleic acid and arachidonic acid concentrations [46], elevate serum anti-oxidative activity and prevent or attenuate decreases in anti-oxidant en‐ zyme activities [44]. In addition to having anti-oxidant properties, green tea catechins have

In particular, Erba et al. (2005) showed a significant decrease in plasma peroxide levels, DNA oxidative damage and LDL oxidation, as well as a significant increase in total anti-oxi‐ dant activity in the plasma of healthy volunteers who consumed two cups of green tea per day in addition to a balanced and controlled diet demonstrating that green tea may act syn‐ ergistically with a correct diet in affecting the biomarkers of oxidative stress [47]. Much of the evidence supporting anti-oxidant functions of tea polyphenols is derived from assays of their anti-oxidant activity *in vitro*. However, evidence that tea polyphenols are acting direct‐

It is very important to underline also that while green tea beverage consumption is con‐ sidered part of a healthy lifestyle, green tea extracts supplements should be used with caution. Very high doses of green tea extracts (6 g–240 g) have been associated with hepa‐ totoxicity in patients who used them for a duration of 5 to 120 days, changing in blood bi‐ ochemical parameters included an elevation of serum levels of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, total bilirubin and albumin levels. Al‐ though, it was observed a reversal of symptoms when subjects stopped taking the green

In addition, in a number of countries, tea is commonly consumed with milk. Interactions be‐ tween tea polyphenols and proteins found in milk have been found to diminish total antioxidant capacity *in vitro*, but it is presently unclear whether consuming tea with milk substantially alters the biological activities of tea flavonoids *in vivo*. The addition of milk to tea did not significantly alter areas under the curve for plasma catechins or flavonols in hu‐ man volunteers, suggesting that adding milk to tea does not substantially affect the bioavail‐

thearubigins [44].

12 Current Trends in Atherogenesis

tea supplement [42].

also been shown to reduce VSMCs proliferation [42].

ly or indirectly as anti-oxidants *in vivo* is more limited [44].

Studies of the herbal medicines for the prevention and treatment of atherosclerosis have re‐ ceived much attention in recent years. Single compounds isolated from some herbal materi‐ als have been shown to reduce the production or remove the build up of cholesterol *in vitro* or *in vivo* studies. Glabrol from Glycyrrhiza glabra has been found to be an acyl-coenzyme A: a cholesterol acyltransferase inhibitor that blocks the esterification and intestinal absorp‐ tion of free cholesterol. Curcumin from Curcuma longa inhibited cholesterol accumulation. Puerarin from Pueraria lobata can promote cholesterol excretion into bile by upregulating the rate-limiting enzyme in the synthesis of bile acid from cholesterol. Moreover, these ex‐ tracts have anti-oxidative effects and may reduce the levels of ox-LDL and increased the lev‐ els of HDL [48].
