The present study was to investigate the mechanisms by which hawthorn fruit lowers serum cholesterol in hamsters. The control group was fed a semisynthetic diet containing 0.1% cholesterol while the tested group was maintained on the same diet but supplemented with 0.5% hawthorn fruit aqueous ethanolic extract for 4 weeks. Serum total cholesterol (TC) and triacylglycerols (TG) were decreased by 10 and 13%, respectively, in hawthorn fruit group as compared with the control (P<0.05). Supplementation of hawthorn fruit aqueous ethanolic extract led to greater excretion of both neutral and acidic sterols. Further enzymatic assays suggest the mechanisms by which hawthorn fruit decreases serum cholesterol involve a greater excretion of bile acids mediated by up-regulation of hepatic cholesterol 7α-hydroxylase (CH) activity, and an inhibition of cholesterol absorption mediated by down-regulation of intestinal acyl CoA:cholesterol acyltransferase (ACAT) activity.

Hawthorn fruit extract has been shown to have many health benefits including being cardiovascular protective, hypotensive and hypocholesterolemic. The present study was carried out to characterize further the antioxidants of hawthorn fruit and their effect on the oxidation of human low density lipoprotein (LDL) and α-tocopherol. The dry hawthorn fruit was extracted successively with ether, ethyl acetate, butanol and water. The ethyl acetate fraction was only effective in inhibition of Cu+2-mediated LDL oxidation. The column chromatographic separation led to isolation of eight pure compounds; namely, ursolic acid, hyperoside, isoquercitrin, epicatechin, chlorogenic acid, quercetin, rutin and protocatechuic acid. All of these phenolic compounds, except ursolic acid, were protective to human LDL from Cu+2-mediated LDL oxidation. They were also effective in preventing the peroxy free radical-induced oxidation of α-tocopherol in human LDL. The inhibitory effect of these compounds on oxidation of LDL and α-tocopherol was dose-dependent at concentrations ranging from 5 to 40µM. In addition, supplementation of 2% hawthorn fruit powder significantly elevated serum α-tocopherol by 18-20% in rats fed a 30% polyunsaturated canola oil diet, as compared with the control. The present results suggest that part of the mechanism for cardiovascular protective effects of hawthorn fruit might also involve the direct protection to human LDL from oxidation or indirect protection via maintaining the concentration of α-tocopherol in human LDL.

Green tea catechins, including (-)-epicatechin (EC), (-)-epicatechin gallate (ECG), (-)-epigallocatechin (EGC) and (-)-epigallocatechin gallate (EGCG), are oxidized and dimerized during the manufacture of black tea and oolong tea to form orange-red pigments, theaflavins (TF), a mixture of theaflavin (TF1), theaflavin-3-gallate (TF2A), theaflavin-3*-gallate (TF2B) and theaflavin-3,3*-digallate (TF3). The present study was designed to compare the antioxidant activities of individual TF with that of each catechin using human LDL oxidation as a model. All catechins and TF tested inhibited Cu12-mediated LDL oxidation. Analysis of the thiobarbituric acid-reactive substances (TBARS) and conjugated dienes produced during LDL oxidation revealed that the antioxidant activity was in the order: TF3>ECG>EGCG≥TF2B≥TF2A>TF1≥ EC>EGC. Four TF derivatives also demonstrated a dose-dependent antioxidant activity in Cu+2-mediated LDL oxidation at concentrations of 5-40mmol/L. These results demonstrate that the TF present in black tea possess at least the same antioxidant potency as catechins present in green tea, and that the conversion of catechins to TF during fermentation in making black tea does not alter significantly their freeradical-scavenging activity. J. Nutr. 131: 2248-2251, 2001.

Green tea catechins (GTCs) as a mixture of (-)-epicatechin (EC), (-)-epicatechin gallate (ECG), (-)-epigallocatechin (EGC), and (-)-epigallocatechin gallate (EGCG) possess a variety of biological activities. We have previously studied the stability of GTCs either as a mixture or as individual epicatechin derivatives in various pH, demonstrating that GTCs as a mixture in alkaline solutions were extremely unstable and degraded almost completely in a few minutes, whereas in acidic solutions (pH<4) they were very stable. For the pH ranging from 4 to 7, the stability of GTCs was inversely associated with the pH value of the incubation solutions. The present study examined the effect of ascorbic acid and citric acid on the stability of GTCs incubated in sodium phosphate buffer (pH =7.42). Ascorbic acid added to the incubation mixture significantly increased the stability of GTCs whereas citric acid exhibited no effect. Four epicatechin derivatives examined demonstrated varying stability, with EGCG and EGC being equally instable and EC and ECG being relatively stable. The addition of ascorbic acid significantly increased the stability of all four derivatives, particularly EGC and EGCG. The present results, although not directly transferable to in vivo conditions, may suggest that the presence of ascorbic acid may stabilize the GTCs in the intestine where the pH is neutral or alkaline before absorption.

This study compared the antioxidative activity of green tea catechin (GTC) extract with that of rosemary extract in canola oil, pork lard, and chicken fat. The GTC extract was obtained from jasmine and longjing green teas and mainly consisted of four epicatechin isomers including (−)epigallocatechin gallate (EGCG), (−)epigallocatechin (EGC), (−)epicatechin (EC), and (−)epicatechin gallate (ECG). The oxidation was conducted at 100±2℃ by monitoring oxygen uptake. The oxygen consumption test demonstrated that GTC extract was much more effective than the rosemary extract against lipid oxidation in canola oil, pork lard, and chicken fat under the conditions of the present study. Together with our previous study which showed that GTC extract was more protective than butylated hydroxytoluene as an antioxidant, these results suggest that GTC as a mixture of EGCG, EGC, EC, and ECG may serve as an antioxidant in processed foods.