Antioxidative activity of naringin and lovastatin in high cholesterol-fed rabbits.

The consumption of a cholesterol-enriched diet increases the degree of lipid peroxidation, which is one of the early processes of atherosclerosis. The aim of this trial was to determine the antioxidative effects of the citrus bioflavonoid, naringin, a potent cholesterol-lowering agent, compared to the cholesterol-lowering drug, lovastatin, in rabbits fed a high cholesterol diet. Male rabbits were served a high-cholesterol (0.5%, w/w) diet or high-cholesterol diet supplemented with either naringin (0.5% cholesterol, 0.05% naringin, w/w) or lovastatin (0.5% cholesterol, 0.03% lovastatin, w/w) for 8 weeks to determine the plasma and hepatic lipid peroxide, plasma vitamin A and E levels, and hepatic hydrogen peroxide levels, along with the hepatic antioxidant enzyme activities and gene expressions. Only the lovastatin group showed significantly lower plasma and hepatic lipid peroxide levels compared to the control group. The naringin supplementation significantly increased the activities of both hepatic SOD and catalase by 33% and 20%, respectively, whereas the lovastatin supplementation only increased the catalase activity by 23% compared to control group. There was no difference in the GSH-Px activities between the various groups. Content of H2O2 in hepatic mitochondria was significantly lower in groups supplemented with lovastatin and naringin than in control group. However, there was no difference in cytosolic H2O2 content in liver between groups. The concentration of plasma vitamin E was significantly increased by the naringin supplementation. When comparing the antioxidant enzyme gene expression, the mRNA expression of SOD, catalase and GSH-Px was significantly up-regulated in the naringin-supplemented group. Accordingly, these results would appear to indicate that naringin, a citrus bioflavonoid, plays an important role in regulating antioxidative capacities by increasing the SOD and catalase activities, up-regulating the gene expressions of SOD, catalase, and GSH-Px, and protecting the plasma vitamin E. In contrast, lovastatin exhibited an inhibitory effect on the plasma and hepatic lipid peroxidation and increased the hepatic catalase activity in high-cholesterol fed rabbits.

Vitamin E improves microsomal phospholipase A2 activity and the arachidonic acid cascade in kidney of diabetic rats.

The purpose of the present study was to investigate the effects of vitamin E on microsomal phospholipase A2 activity and the arachidonic acid cascade in the kidneys of streptozotocin (STZ)-induced diabetic rats. Sprague-Dawley male rats weighing 100 +/- 10 g were randomly assigned to one normal and three STZ-induced diabetic groups. The diabetic groups were fed a vitamin E-free diet (the DM-0E group), 40 mg vitamin E/kg diet (the DM-40E group) or a 400 mg vitamin E/kg diet (the DM-400E group). The kidney vitamin E concentrations were 59 and 49% lower in the DM-0E and DM-40E groups, respectively, than in the normal group. The kidney thiobarbituric acid reactive substance concentrations in the DM-0E, DM-40E and DM-400E groups were 119, 84 and 33% greater, respectively, than that in the normal group. The concentration in the DM-400E group was 39% lower than that in the DM-0E group. The phospholipase A2 (PLA2) activity in the kidney microsomes of the DM-0E-40E and DM-400E groups were 88, 58 and 35% greater, respectively, than that in the normal group. The activity in the DM-400E group was 28% lower than that in the DM-0E group and 16% lower than that in the DM-40E group. The differences in the phospholipids in the kidney microsomes included reductions in the phosphatidylcholine and phosphatidylethanolamine compositions. Phosphatidylethanolamine hydrolysis in the kidney microsomes of the DM-0E and DM-40E groups were 84 and 64%, which did not differ from the DM-400E group. The formation of thromboxane A2 (TXA2) in the kidney microsomes was 137 and 70% greater in the DM-0E and DM-40E groups, respectively, than in the normal group. TXA2 formation did not differ between the DM-400E and normal groups. The formation of prostacyclin in the kidney microsomes was 60 and 44% lower in the DM-0E and DM-40E groups, respectively, than in the normal group, whereas the DM-400E group did not differ from that in the normal group. The ratio of prostacyclin to TXA2 was 82 and 65% lower than normal in the DM-0E and DM-40E groups, respectively. Kidney function appears to be improved by vitamin E supplementation due to its antithrombus action, which in turn controls the arachidonic acid cascade system.

Effects of green tea catechin on phospholipase A2 activity and antithrombus in streptozotocin diabetic rats.

The purpose of this study was to investigate the effects of dietary green tea catechin on phospholipase A2 (PLA2) activity and the antithrombotic reaction of platelets in streptozotocin (STZ)-diabetic rats. Sprague-Dawley male rats weighing 100 +/- 10 g were randomly divided into one normal and three STZ-diabetic groups, which were subdivided into catechin-free group (DM-0C), 0.5% catechin group (DM-0.5C) and 1% catechin group (DM-1C). The activity level of platelet phospholipase A2 was higher in the diabetic groups than in the normal group, while it was lower in DM-0.5C and DM-1C than in DM-0C. The activity of platelet cyclooxygenase in DM-0C was 1.1-fold as high as in the normal group, but was significantly reduced by catechin supplementation. The platelet thromboxane A2 (TXA2) formation became higher in DM-0C as compared to the normal group, but not in DM-0.5C and DM-1C. The synthesis of aortic prostacyclin (PGI2) was lower in DM-0C and DM-0.5C than in the normal group. The PGI2/TXA2 ratio was decreased to 55% in DM-0C, but was restored by catechin supplementation. These results indicate that STZ-diabetic rats are sensitive to platelet aggregation and thrombosis, and that the abnormality can be improved by dietary catechin.

Effects of green tea catechin on hepatic microsomal phospholipase A2 activities and changes of hepatic phospholipid species in streptozotocin-induced diabetic rats.

In this study, male Sprague-Dawley rats weighing 70 +/- 5 g were divided into a control (normal) group and three different diabetes mellitus (DM) groups that were supplemented with catechin-free (DM-0C), 0.5% catechin dietary (DM-0.5C), and 1% catechin (DM-1.0C). The animals were maintained on an experimental diet for four weeks. At this point, they were injected with streptozotocin (STZ) to induce diabetes, and they were sacrificed on the 6th day to determine the activities of phospholipase A2 (PLA2) and the changes of phospholipid species by catechin supplementation. In liver tissues, no significant differences were found between the PC hydrolysis of a normal group and a diabetic group; however, PE hydrolysis of the DM-0C, DM-0.5C, and DM-1.0C groups increased by 68.9%, 34.01%, and 26.9%, respectively, compared with the normal group. Although the PLA2 activity of the DM-0C group in the liver tissues increased 91% compared with the normal group, the PLA2 activity of DM-0.5C and DM-1.0C, which were fed catechin, increased 50% and 56%, respectively, compared with the normal group. In the liver tissues, peroxide values of the DM-0C, the DM-0.5C, and the DM-1.0C groups were increased 109%, 32.8%, and 46.7%, respectively, compared with the normal group. Based on these results for STZ-induced diabetic rats, lipid peroxidation seems to be accelerated specifically with the increased PLA2 activities. Thus if antioxidants like catechin were supplementation, the activity of PLA2 and PE hydrolysis can be altered and the accumulation of lipid peroxide would be decreased. Therefore we concluded that the antioxidant catechin for diabetic animals can significantly reduce PLA2 activities and lipid peroxide formation.