Effects of the Cellcultured Acanthopanax senticosus Extract on Antioxidative Defense System and Membrane Fluidity in the Liver of Type 2 Diabetes Mouse.

This study examined the effect of cellcultured Acanthopanax senticosus (A. senticosus) extract on the antioxidative defense system, oxidative stress and cell membrane fluidity in the liver of type 2 diabetes in the C57BL/6J mouse as an animal which is genetically prone to develop insulin resistance and obesity/diabetes. C57BL/6J mice were randomly divided, control diet (N-C), high fat diet (DM-C), control diet plus A. senticosus extract (N-CASM), and high fat diet plus A. senticosus extract (DM-CASM). The mice were orally administered an A. senticosus extract (0.5 g/kg body weight) in the N-CASM and DM-CASM groups once a day for 12 weeks, and distilled water in the N-C and DM-C groups. Cellcultured A. senticosus extract was found to be excellent for strengthening the antioxidative defense system, reducing the generation of reactive oxygen species (ROS) and damaging oxidative substances, and maintaing membrane fluidity (MF) in the liver of type 2 diabetes mouse.

Physiological function of insoluble dietary fiber prepared from exploded oak wood (Quercus mongolica).

This study investigated the production of insoluble dietary fiber using exploded and chemically treated oak wood (Quercus mongolica) and the physiological functions of prepared insoluble dietary fiber in laboratory animals. To produce high quality insoluble dietary fiber, the steam explosion treatment was performed at 25 kgf/cm2 pressure for 6 minutes. In the chemical analysis of insoluble dietary fiber, exploded oak wood was pretreated by 1% sodium hydroxide solution. The insoluble dietary fiber contained 7.6% residual lignin and 61.7% of alpha-cellulose. In order to compare the physiological functions of prepared insoluble dietary fiber with those of commercial insoluble dietary fiber, Sprague-Dawley male rats weighing 100 +/- 10 g were randomly assigned to one normal diet and five high cholesterol diets, containing 1% cholesterol. The high cholesterol diet groups were classified as the fiber-free diet (FF group), 5% commercial alpha-cellulose diet group (5C group), 10% commercial alpha-cellulose group (10C group), 5% insoluble dietary fiber group (5M group) and 10% insoluble dietary fiber group (10M group). Food intake, weight gain and food efficiency ratio in high cholesterol groups were significantly higher than those of the normal group, but there were no significant differences among the high cholesterol diet groups. In addition, there were no significant differences in the weights of liver, kidney and small intestine in insoluble dietary fiber-supplemented groups. Cecum weights in all insoluble dietary fiber groups were significantly higher than those of the FF group. There were no significant differences in the activities of the glutamic pyruvic transaminase (GPT) and glutamic oxaloacetic transaminase (GOT) among the insoluble dietary fiber-supplemented groups. In conclusion, the prepared insoluble dietary fiber and the commercially available insoluble fiber showed the same physiological effects. Moreover, the preparation method for the insoluble dietary fiber from the exploded oak wood was successful.

Effects of vitamin E on phospholipase A2 activity and oxidative damage to the liver in streptozotocin-induced diabetic rats.

BACKGROUND: The purpose of the present study was to investigate the effects of vitamin E on oxidative stress and cell membrane fluidity in the liver of streptozotocin (STZ)-induced diabetic rats. METHODS: Sprague-Dawley male rats weighing 100 +/- 10 g were fed a vitamin E-free diet (the DM-0E group), a 40 mg vitamin E/kg diet (the DM-40E group), or a 400 mg vitamin E/kg diet (the DM-400E group). RESULT: Dietary vitamin E reduced the increased concentration of lipid peroxides in the liver tissues of diabetic rats through decreasing their increased phospholipase A(2) (PLA(2)) activity and phosphatidylethanolamine hydrolysis. However, vitamin E reduced the accumulation of superoxide radical and decreased the generation of oxidative damage substances, such as the carbonyl value, increased membrane fluidity and lowered oxidative damage. CONCLUSIONS: Vitamin E was found to be excellent for regulating the activity of PLA(2), reducing the generation of reactive oxygen species and damaging oxidative substances, and maintaining cell membrane fluidity in the liver of diabetic rats.

Green tea catechins protect rats from microwave-induced oxidative damage to heart tissue.

We investigated the effects of green tea catechin on oxidative damage in microwave-exposed rats. The microwave-exposed rats received one of three diets: catechin-free (MW-0C), 0.25% catechin (MW-0.25C), or 0.5% catechin (MW-0.5C). Rats were sacrificed 6 days after microwave irradiation (2.45 GHz, 15 minutes). Cytochrome P(450) levels in the MW-0C group was increased by 85% compared with normal, but was 11% and 14% lower in the MW-0.25C and MW-0.5C groups than in the MW-0C group. NADPH-cytochrome P(450) reductase activity in the MW-0C group was increased by 29%, compared with the normal group, but was significantly less in the MW-0.25C and MW-0.5C groups. Superoxide dismutase activity in the MW-0C group was decreased by 34%, compared with the normal group, but in the MW-0.25C and MW-0.5C groups was 19% and 25% higher. The activity of glutathione peroxidase in the MW-0C group was decreased by 28% but remained near normal with catechin supplements. Superoxide radical concentrations in the MW-0C group were increased by 35%, compared with the normal group. However, superoxide radicals in the MW-0.25C and MW-0.5C groups were 11% and 12% lower, respectively, compared with the MW-0C group. Microwave irradiation significantly increased levels of thiobarbituric acid-reactive substances, carbonyl values, and lipofuscin contents, but green tea catechin partially overcame the effects of the microwave irradiation. In conclusion, the mixed function oxidase system was activated, the formation of superoxide radical, lipid peroxide, oxidized protein, and lipofuscin was increased, and the antioxidative defense system was weakened in heart tissue of microwave-exposed rats, but the oxidative damage was significantly reduced by catechin supplementation.

Effects of green tea catechin on polymorphonuclear leukocyte 5'-lipoxygenase activity, leukotriene B4 synthesis, and renal damage in diabetic rats.

The purpose of this study was to investigate the effects of green tea catechin on polymorphonuclear leukocyte 5'-lipoxygenase activity, leukotriene B4 synthesis, and renal damage in diabetic rats. Male Sprague-Dawley rats weighing 100 +/- 10 g were randomly assigned to 1 normal group and 3 diabetic groups given a catechin-free diet (DM-0C group), 0.25% catechin diet (DM-0.25C group), or 0.5% catechin diet (DM-0.5C group), respectively. 5'-Lipoxygenase activity in the polymorphonuclear leukocytes significantly increased by 54% in the DM-0C group compared to the normal group, while the level in the DM-0.5C group remained the same as in the normal group. The leukotriene B4 content in the polymorphonuclear leukocytes increased 55% in the DM-0C group compared to the normal group, whereas the DM-0.25C and DM-0.5C groups exhibited the same level as the normal group. The superoxide radical content in the kidney microsomes increased 116% in the DM-0C group when compared to the normal group, yet decreased 29% in the DM-0.25C group and 50% in the DM-0.5C group compared to DM-0C group. The lipofuscin content was 197 and 136% higher in the DM-0C and DM-025C groups, respectively, than in the normal group, whereas the DM-0.5C group exhibited the same content as in the normal group. The carbonyl value increased 118% in the DM-0C group compared to the normal group, and the DM-0.25C and DM-0.5C groups were not significantly different from the DM-0C group. Accordingly, these results indicate that dietary catechin inhibited the generation of superoxide radicals, oxidized protein, and lipid peroxide in the kidney of streptozotocin-induced diabetic rats. Furthermore, green tea catechin supplementation in diabetic rats also appeared to inhibit the production of leukotriene B4 based on regulating the activity of 5'-lipoxygenase, thereby potentially reducing renal oxidative damage and inflammatory reactions.

Effects of vitamin E on oxidative stress and membrane fluidity in brain of streptozotocin-induced diabetic rats.

BACKGROUND: Diabetics and experimental animal models exhibit high oxidative stress due to persistent and chronic hyperglycemia, thereby deplete the activity of the antioxidative defense system and thereby promote the generation of free radicals. The current study examined the effects of vitamin E on oxidative stress and membrane fluidity in the brain of diabetes-induced rats. METHODS: Sprague-Dawley male rats were randomly assigned to normal and streptozotocin (STZ)-induced diabetic groups. The diabetic groups were fed a vitamin E-free diet, 40 mg vitamin E/kg diet, or 400 mg vitamin E/kg diet. Diabetes was induced with STZ after 3 weeks of the experimental diet, then the rats were sacrificed 9 days later to determine the oxidative stress and cell membrane fluidity in the brain. RESULTS: Dietary vitamin E strengthened the antioxidative defense system with an increased activity of the antioxidant enzymes, such as superoxide dismutase (SOD) and glutathione peroxidase (GSH-px) and increased vitamin E content, in the brain of the diabetes-induced experimental rats. Accordingly, vitamin E was found to reduce the accumulation of reactive oxygen species (ROS), such as superoxide radical decrease the generation of oxidative damage substances, such as the carbonyl value, increase the membrane fluidity lowered by oxidative damage, and significantly improve the lipid composition. CONCLUSIONS: Vitamin E was found to be excellent for strengthening the antioxidative defense system, reducing the generation of ROS and damaging oxidative substances, and maintaining membrane fluidity in the brain of diabetes-induced rats.

Effects of forsythia fruit extracts and lignan on lipid metabolism.

A primary methanol extract (F-ME), secondary butanol-soluble fraction (F-BU), and lignans were prepared from forsythia fruit (Forsythia viridissima L.) and added to 0.5% (w/w) cholesterol diets for male Sprague-Dawley rats weighing 121 +/- 12 g. There were six experimental groups: a control group, 0.2%, 0.4% F-ME supplemented groups, 0.1%, 0.02% F-BU groups and 0.02% lignan group. After 3 weeks of feeding, body weight gains, serum GOT and GPT levels were not different among the groups. HDL-/total cholesterol ratios increased in the 0.2% F-BU and lignan groups compared with the control groups. Liver triglyceride level lowered in most of forsythia groups. Fecal cholesterol excretions increased in the lignan group. Arctiin isolated from the forsythia fruit reduced cholesterol and triglyceride contents in cultured HepG2 cells at 0.01-0.1 microM. These results indicated that the forsythia lignan, arctiin is effective on improving blood lipid status without a significant hepatotoxicity and is to be utilized for the functional foods for lipid-lowering action.

Acanthopanax senticosus extract prepared from cultured cells decreases adiposity and obesity indices in C57BL/6J mice fed a high fat diet.

The herb Acanthopanax senticosus was cultured from a cell suspension by a proprietary process, and evaluated for protective effects against obesity in C57BL/6J mice fed high fat diets. Forty 4-week-old male C57BL/6J mice (n = 10) were fed either a normal diet (10 kcal fat%) or high fat diet (60 kcal fat%) given with or without oral administration of A. senticosus extract (ASE; 0.5 g/kg of body weight) for 12 weeks. Feed consumption was not different among the groups, but energy intake was higher in the groups fed high fat diets than in the groups fed normal diets. Body weight gain, abdominal fat accumulation, and serum leptin concentrations were significantly higher in the high fat-fed groups than the other groups. Animals fed the high fat diet had significantly higher low-density lipoprotein (LDL)-cholesterol in serum and higher triglyceride accumulation in liver, but the ASE supplement restored both to the same levels as in the animals fed low fat diets. Total carnitine concentration were not significantly different between the two diet groups; also the oral administration of ASE did not alter carnitine status. Accordingly, the current results suggest the oral administration of ASE seemed to lower the weight gain, serum LDL-cholesterol concentration, and liver triglycerides accumulation in mice with obesity induced by high fat diets. These results seemed to suggest that supplementation with ASE might have a role in the prevention of obesity in high fat-fed mice.

Effects of vitamin E on renal dysfunction in chronic cadmium-poisoned rats.

Cadmium is a highly toxic metal that can be ingested or inhaled from a variety of industrial and dietary sources. The purpose of this study was to investigate the effects of vitamin E on renal dysfunction and blood pressure changes in chronic cadmium-poisoned rats. Sprague-Dawley rats weighing 100 +/- 10 g were randomly assigned to one control group and three cadmium-poisoned groups. Cadmium groups were assigned to dietary groups according to levels of vitamin E supplementation: vitamin E-free diet (Cd-0E group), 40 mg of vitamin E/kg of diet (Cd-40E group), and 400 mg of vitamin E/kg of diet (Cd-400E group). The animals were raised for 20 weeks, and cadmium was supplied in the drinking water at 50 ppm Cd(2+). The morphological changes observed by both light and electron microscopy revealed mitochondria and tubule epithelial cell edema in the Cd-0E group, yet this was alleviated with the highest level of vitamin E supplementation (Cd-400E group). The urinary beta(2)-microglobulin levels indicated that glomerular injury was higher in the Cd-poisoned groups than in the control group, but were lowered by vitamin E supplementation. Although the glomerular filtration rate (GFR) of the Cd-0E group was significantly lower than that of the control group, the vitamin E-supplemented groups exhibited a similar GFR to the control group, suggesting that vitamin E protected the kidney from functional damage. Angiotensin converting enzyme activity, and blood pressure, and heart rate were all significantly higher in the Cd-poisoned group, but each remained nearly normal with vitamin E supplementation. Accordingly, these results indicate that vitamin E supplementation in chronic cadmium-poisoned rats normalized renal dysfunction and blood pressure regulation.

Action of green tea catechin on bone metabolic disorder in chronic cadmium-poisoned rats.

The purpose of this study was to investigate the effects of green tea catechin on bone metabolic disorders and its mechanism in chronic cadmium-poisoned rats. Sprague-Dawley male rats weighing 100+/-10 g were randomly assigned to one control group and three cadmium-poisoned groups. The cadmium groups included a catechin free diet (Cd-0C) group, a 0.25% catechin diet (Cd-0.25C) group and a 0.5% catechin diet (Cd-0.5C) group according to their respective levels of catechin supplement. After 20 weeks, the deoxypyridinoline and crosslink values measured in urine were significantly increased in the Cd-0C group. Cadmium intoxication seemed to lead to an increase in bone resorption. In the catechin supplemented group (Cd-0.5C group), these urinary bone resorption marks, were decreased. The serum osteocalcin content in the cadmium-poisoned group was significantly increased as compared with the control group. In the catechin supplemented group serum osteocalcin content values were lower than the control group. The cadmium-intoxicated group (Cd-0C group), had lower bone mineral density than the control group (total body, vertebra, pelvis, tibia and femur). The catechin supplement increased bone mineral density to about the same as the control group. Bone mineral content showed a similar trend to total bone mineral density. Therefore, the bone mineral content of the Cd-0C group at the 20th week was significantly lower than the control group. The catechin supplemented group (Cd-0.5C group) was about the same as the control group. The cause of decreasing bone mineral density and bone mineral content by cadmium poisoning was due to the fast bone turnover rate, where bone resorption occurred at a higher rate than bone formation. The green tea catechin aided in normalizing bone metabolic disorders in bone mineral density, bone mineral content and bone calcium content caused by chronic cadmium intoxication.

Effects of manufactured soluble dietary fiber from Quercus mongolica on hepatic HMG-CoA reductase and lipoprotein lipase activities in epididymal adipose tissue of rats fed high cholesterol diets.

This study investigated the effect of a manufactured soluble dietary fiber on lipid metabolism in rats fed high cholesterol diets. Soluble dietary fiber was prepared from wood chips of oak (Quercus mongolica). Male Sprague-Dawley rats weighing 100 +/- 10 g were randomly assigned to either a normal diet or five high cholesterol diets containing 1% cholesterol and different fiber supplements. The high cholesterol groups were subdivided into fiber-free diet (FF), 5% pectin (5P), 10% pectin (10P), 5% manufactured soluble dietary fiber (5QM), and 10% manufactured soluble dietary fiber (10QM) groups. Total serum cholesterol concentrations in all soluble dietary fiber-supplemented groups were lower than in the FF group. The high-density lipoprotein-cholesterol concentration in the FF group was significantly lower, compared with the normal group, but was increased in groups supplemented with soluble dietary fiber. Low-density lipoprotein-cholesterol levels and the atherogenic index had the same tendency as total cholesterol concentration. Compared with the FF group, in the 5P, 5QM, 10P, and 10QM groups hepatic triglyceride concentrations were 12%, 16%, 20%, and 24% lower, respectively, and hepatic cholesterol concentrations were 48%, 52%, 52%, and 58% lower, respectively. Hepatic 3-hydroxy-3-methylglutaryl-CoA reductase activity in the soluble fiber groups was significantly higher than in the FF groups, but lower than the normal group. When hepatic tissue was observed under a light microscope, the FF group had completely formed lipomas in the hepatic tissue, which led to fat deposits and then a fatty liver. The size and number of lipomas were lower in the soluble dietary fiber-fed groups, as compared with the group not fed dietary fiber. In conclusion, improvements in lipid metabolism were observed as a result of the manufactured soluble dietary fiber from the oak chips, and were similar to that seen for pectin. The preparation method for the soluble dietary fiber from oak chips successfully produced a functional soluble fiber.

Effect of green tea catechin on arachidonic acid cascade in chronic cadmium-poisoned rats.

The purpose of this study was to investigate the effect of green tea catechin on the cyclooxygenase and lipoxygenase pathways in chronic cadmium-poisoned rats. Sprague-Dawley male rats weighing 100 +/- 10 g were randomly assigned to one normal and three cadmium-poisoned groups. The cadmium groups were classified as catechin-free diet group (Cd-0C), 0.25% catechin diet group (Cd-0.25C) and 0.5% catechin diet group (Cd-0.5C), in accordance with the level of catechin supplement. The phospholipase A2 activity was remarkably increased 117% in the Cd-0C group and 60% in the Cd-0.25C group compared with the normal group, and the level in the Cd-0.5C group was the same as the normal group. Activity of platelet cyclooxygenase increased 284% in the Cd-0C group, 147% in the Cd-0.25C group and 193% in the Cd-0.5C group. The synthesis of platelet thromboxane A2 (TXA2) increased 157% in the Cd-0C group and 105% in the Cd-0.25C group, compared with the normal group. The Cd-0.5C group showed the same level as the normal group. Prostacyclin (PGI2) formation in the aorta decreased 24% in the Cd-0C group and 18% in the Cd-0.25C group. The ratio of PGI2/TXA2, the thrombocyte synthesis index, decreased 70% in the Cd-0C group and 59% in the Cd-0.25C group. The activity of 5'-lipoxygenase in the polymorphonuclear leukocyte was increased 40% in the Cd-0C group as compared with the normal group. Catechin-supplemented Cd-0.25C and Cd-0.5C groups showed the level of the normal group. In this study, the observed content of leukotriene B4, which induces the inflammatory process, increased 54% in the Cd-0C group, and in catechin-supplemented groups, showed the same level as in the normal group. The serum peroxide value increased 60% in the Cd-0C group compared with the normal group; but in the Cd-0.5C group, it showed the level of the normal group. These results indicate that chronic cadmium poisoning in rats accelerates arachidonic acid metabolism. Inhibition of arachidonic acid metabolism due to catechin supplementation, however, decreases platelet aggregation and inflammatory action. In conclusion, it would appear that green tea catechin supplementation in chronic cadmium-poisoned rats inhibits the arachidonic acid cascade by regulating the activity of phospholipase A2.

Green tea catechin improves microsomal phospholipase A2 activity and the arachidonic acid cascade system in the kidney of diabetic rats.

The purpose of this study was to investigate the effects of green tea catechin on the microsomal phospholipase A2 activity and arachidonic acid cascade in the kidneys of streptozotocin-induced diabetic rats. Sprague-Dawley male rats weighing 100 +/- 10 g were assigned randomly to one normal and three streptozotocin-induced diabetic groups. The diabetic groups were the DM-0C group (n = 10), fed a catechin-free diet, the DM-0.25C group (n = 10), fed a 0.25 g catechin per 100 g diet, and the DM-0.5C group (n = 10), fed a 0.5 g catechin per 100 g diet. The kidney microsomal phospholipase A2 activity was higher in the diabetic groups than in the normal group, while it was lower in the DM-0.25C and DM-0.5C groups than in the DM-OC group. The percentage of phosphatidylcholine hydrolysed in the kidney microsomes was not significantly different between any of the four groups. The percentage of phosphatidylethanolamine hydrolysed in the kidney microsomes was progressively higher in the DM-0.5C, DM-0.25C and DM-OC groups, respectively, compared to the normal group. The formation of thromboxane A2 was significantly higher while the formation of prostacyclin was lower in kidney microsomes of the streptozotocin-induced diabetic groups compared with the normal group, but this condition was improved by catechin supplementation. Kidney microsomal vitamin E concentrations were progressively lower in the DM-0.5C, DM-0.25C, and DM-0C groups, respectively, compared to the normal group. The kidney thiobarbituric acid reactive substance (TBARS) contents became higher in the DM-0C and DM-0.25C groups as compared with the normal group, whereas the DM-0.5C group did not differ from the normal group. Kidney function appears to be improved by green tea catechin supplementation due to its antithrombus action, which in turn controls the arachidonic acid cascade system.

Effects of green tea catechin on prostaglandin synthesis of renal glomerular and renal dysfunction in streptozotocin-induced diabetic rats.

The purpose of the present study was to investigate the effects of green tea catechin on prostaglandin synthesis of renal glomerular and renal dysfunction in rats with streptozotocin-induced diabetes. Sprague-Dawley rats weighing 100 +/- 10 g were randomly assigned to one normal group and three groups with streptozotocin-induced diabetes. The diabetic groups were classified to a catechin-free diet (DM group), a 0.25% catechin diet (DM-0.25C group) and a 0.5% catechin diet (DM-0.5C group) according to the levels of catechin supplement in their diet. The animals were maintained on an experimental diet for 4 weeks. At this point, they were injected with streptozotocin to induce diabetes. They were killed on the sixth day. The catechin supplementation groups (DM-0.25C, DM-0.SC groups) showed a decrease in thromboxane A2 synthesis but an increase in prostacyclin synthesis, compared to the DM group. The ratio of prostacyclin/thromboxane A2 was 53.3% and 38.1% lower in the DM and DM-0.25C groups, respectively, than in the normal group. The ratio in the DM-0.5C group did not differ from that in the normal group. The glomerular filtration rate in catechin feeding groups (DM-0.25C and DM-0.5C groups) was maintained at the normal level. The urinary beta2-microglobulin content in the DM-0.5C group was significantly lower than that in the normal group. On the sixth day after induction of diabetes, the urinary microalbumin content in the DM, DM-0.25C and DM-0.5C groups had increased 5.40, 4.02, 3.87 times, respectively, compared with the normal group. In conclusion, kidney function appears to be improved by green tea catechin supplementation due to its antithrombotic action, which in turn controls the arachidonic acid cascade system.