• Nutrition Research and Practice
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• v.13 no.5
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• pp.377-383
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• 2019

BACKGROUND/OBJECTIVES: Hyperglycemia-induced hepatic damage has been recognized as one of the major cause of complications in diabetes. Hepatic complications are associated with inflammation and oxidative stress in diabetes. In this study, we investigated the hypothesis that gamma-tocopherol (GT) supplementation ameliorates NLRP3 inflammasome associated hepatic inflammation in diabetes. MATERIALS/METHODS: Diabetes was induced by the intraperitoneal injection of alloxan (150 mg/kg. BW) in ICR mice. All mice were fed with a control diet (AIN-76A). After diabetes was induced (fasting glucose level ${\geq}250mg/dL$), the mice were treated with tocopherol-stripped corn oil or GT-supplemented (35 mg/kg) corn oil, respectively, by gavage for 2 weeks. RESULTS: GT supplementation reduced fasting blood glucose levels in diabetic mice relative to non-treated diabetic mice. Moreover, GT supplementation ameliorated hyperglycemia-induced hepatic damage by regulation of NOD-like receptor protein 3 (NLRP3)-inflammasome associated inflammation represented by NLRP3, apoptosis-associated speck-like protein containing a caspase-recruitment domain, caspase-1, nuclear $factor-{\kappa}B$ pathway as well as oxidative stress demonstrated by nuclear factor erythroid 2-related factor 2, NAD(P)H dehydrogenase quinone 1, catalase and glutathione-dependent peroxidase in diabetic mice. CONCLUSION: The findings suggested that GT supplementation ameliorated hepatic damage by attenuating inflammation and oxidative stress in alloxan-induced diabetic mice. Taken together, GT could be a beneficial nutrient that can ameliorate inflammatory responses associated with NLRP3 inflammasome in hyperglycemia-induced hepatic damage.

• Asian-Australasian Journal of Animal Sciences
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• v.21 no.8
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• pp.1164-1170
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• 2008

In this study, the effects of propolis and vitamin C (L-ascorbic acid) supplementation in diets were investigated on feed intake (FI), body weight (BW), body weight gain (BWG), feed conversion rate (FCR) and digestibility and on egg production and qualities (weight, mortality, shell thickness) in laying hens exposed to heat stress. A total of 150 Hyline White Leghorn, aged 42 weeks, hens was divided into five groups of 30 hens. Chicks were randomly divided into 1 positive control, 1 control and 3 treatment groups. The chicks were kept in cages in temperature-controlled rooms at $22^{\circ}C$ for 24 h/d (positive control, Thermoneutral, TN group) or $34^{\circ}C$ for 9 h/d from 08.00-17.00 h followed by $22^{\circ}C$ for 15 h (control, heat stress, HS group) and fed a basal diet or basal diet supplemented with vitamin C (250 mg/kg of L- ascorbic acid/kg of diet) or two levels of propolis (2 and 5 g of ethanol extracted propolis/kg of diet). Increased FI (p<0.05) and improvement in FCR (p<0.05), hen day egg (p<0.05) and egg weight (p<0.05) were found in Vitamin C and propolis-supplemented laying hens reared under heat stress conditions. Mortality rate was higher in the control group than TN, vitamin C and propolis groups (p<0.05). Digestibility of dry matter, organic matter, crude protein and ether extract improved with increasing of both dietary vitamin C and propolis (p<0.05). Vitamin C or propolis supplementation did not affect either the percentage shape index, yolk index or haugh unit and albumen index (p>0.05). However, the egg shell thickness and egg shell weight appeared to be increased in Vitamin C and propolis groups in comparison to HS group birds (p<0.05). In conclusion, dietary supplementation of laying hens with anti-oxidants (vitamin C and propolis) can attenuate heat stress-induced oxidative damage. These positive effects were evidenced by increased growth performance and digestibility, improvement of egg shell thickness and egg weight in comparison to non-supplemented birds. Moreover, supplementation with propolis (5 g/kg diet) was the most efficient treatment.

• Asian-Australasian Journal of Animal Sciences
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• v.28 no.2
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• pp.171-179
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• 2015

The present study was aimed at investigating the adverse effects of dietary zearalenone (ZEA) (1.1 to 3.2 mg/kg diet) on serum hormones, morphologic and apoptotic measurements of genital organs in post-weaning gilts. A total of twenty gilts ($Landrace{\times}Yorkshire{\times}Duroc$) weaned at 21 d with an average body weight of $10.36{\pm}1.21kg$ were used in the study. Gilts were fed a basal diet with an addition of 0, 1.1, 2.0, or 3.2 mg/kg purified ZEA for 18 d ad libitum. Results showed that 3.2 mg/kg ZEA challenged gilts decreased (p<0.05) the serum levels of luteinizing hormone, however, serum levels of prolactin in gilts fed the diet containing 2.0 mg/kg ZEA or more were increased (p<0.05) compared to those in the control. Linear effects on all tested serum hormones except progesterone were observed as dietary ZEA levels increased (p<0.05). Gilts fed ZEA-contaminated diet showed increase (p<0.05) in genital organs size, hyperplasia of submucosal smooth muscles in the corpus uteri in a dose-dependent manner. However, the decreased numbers of follicles in the cortex and apoptotic cells in the ovarian were observed in gilts treated with ZEA in a dose-dependent manner. Degeneration and structural abnormalities of genital organs tissues were also observed in the gilts fed diet containing 1.1 mg/kg ZEA or more. Results suggested that dietary ZEA at 1.1 to 3.2 mg/kg can induce endocrine disturbance and damage genital organs in post-weaning gilts.

• Herbal Formula Science
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• v.8 no.1
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• pp.129-146
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• 2000

This study was carried out to investigate the effects of Solanum lyratum Extract (SLE) on the recovery of liver in $CCI_{4}-intoxicated$ mice. In this study, ICR-Mice were divided into 3 experimental groups; Normal group was fed basal diet and was fed bassal diet for 2 Weeks, sample group was injected $CCl_{4}\;(0.6m{\ell}/kg)$ and was fed basal diet for 2 weeks, sample group was injected $CCl_{4}\;(0.6m{\ell}/kg)$ and was fed the SLE 500mg/kg fod 2 Weeks. In sample group, the level of serum AST, ALT, ALP activity decreased significantly compared with control group. This results suggest that SLE has appreciable therapeutic effect on $CCI_4$ induced hepatotoxicity. In sample group, the level of LPO in liver homogenates decreased significantly compared with control group. In sample group. the level of GSH, catalase in liver homogenates increased significantly compared with control group. This results suggest that SLE has appreciable antioxidant effect on $CCI_4induced hepatotoxicity. In conclusion the results suggest that SLE has appreciable therapeutic effect and antioxidant effect on $CCI_4$ induced hepatotoxicity.

• Journal of Nutrition and Health
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• v.34 no.5
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• pp.525-531
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• 2001

The present study investigated the protective effects of green tea against acute ethanol-induced lipid peroxidation and the change of antioxidative enzyme activities in various regions of rat brain : cortex, cerebellum, striatum and hippocampus. The following parameters were examined : malondialdehyde(MDA) levels and activities of superoxide dismutase(SOD), catalase and glutathione peroxidase(GSH-Px). Male Sprague-Dawley rats were given the experimental containing 1% green tea powder or control diet for 4 weeks, and at the end of feeding diet group received acute ethanol(5g/kg body weight) or equicaloric sucrose solution intragastrically. Green tea powder significantly decreased MDA levels in the striatum compared to control-non alcohol treated group to 1% green tea-non alcohol treated group without altering the antioxidative enzyme activities. Green tea resulted in a significant increase in GSH-Px activities in the hippocampus compared to either control-non alcohol treated group(0.043units/mg protein) or 1% green tea-non alcohol treated group(0.071units/mg protein). In conclusion, these results suggest that moderate consumption of green tea leaves can exert protective effects against ethanol-induced oxidative stress in brain regions, by reducing MDA concentrations in the striatum and enhancing GSH-Px activities in the hippocampus. (Korean J Nutrition 34(5) : 525∼531, 2001)

• Journal of the Korean Society of Food Science and Nutrition
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• v.27 no.1
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• pp.149-156
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• 1998

The purpose of this study was to investigate the effects of vitamin E supplementation on the activities of antioxidative enzymes in liver of KK mice of various ages and various duration of diabetes. Diabetes was induced by feeding high fat diet containing 20% corn oil(wt/wt). Weaned KK mice were fed high fat diet containing 51 IU or 2080 IU vitamin E per kg diet. Animals were sacrificed at 4, 6, and 9 months of age. In nondiabetic group, we found the decrease of antionxidative enzyme activities with aging. In diabetic group, antioxidative enzyme activities were decreased, and the change of hepatic vitamin E was related to glutathione peroxidase activity (r=0.71, p<0.001). Treatment with vitamin E did not modify the level of fasting blood glucose. However, it was observered that glutathione reductase and glutathione peroxidase activities as well as hepatic glutathione levels were increased by vitamie E supplementation, whereas catalase activity did not changed. The present result suggest that high vitamin E supplementation protects against lipid peroxidative damage in diabetic KK mice.

• Toxicological Research
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• v.35 no.4
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• pp.403-410
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• 2019

Curcumin, a hydrophobic polyphenol isolated from the Curcuma longa L. plant, has many pharmacological properties, including antioxidant, anti-inflammatory, and chemo-preventive activities. Curcumin has been shown to have potential in preventing nonalcoholic fatty liver disease (NAFLD). However, the low bioavailability of curcumin has proven to be a major limiting factor in its clinical adoption. Theracurmin, a highly bioavailable curcumin that utilizes micronized technology showed improved biological absorbability in vivo. The aim of this study was to investigate the role of theracurmin in modulating hepatic lipid metabolism in vivo. A fatty liver mouse model was produced by feeding mice a high fat diet (HFD; 60% fat) for 12 weeks. We found that treatment for 12 weeks with theracurmin significantly lowered plasma triacylglycerol (TG) levels and reduced HFD-induced liver fat accumulation. Theracurmin treatment lowered hepatic TG and total cholesterol (T-CHO) levels in HFD-fed mice compared to controls. In addition, theracurmin administration significantly reduced lipid peroxidation and cellular damage caused by reactive oxygen species in HFD-fed mice. Overall, these results suggest that theracurmin has the ability to control lipid metabolism and can potentially serve as an effective therapeutic remedy for the prevention of fatty liver.

• Journal of the Korean Society of Food Science and Nutrition
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• v.22 no.6
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• pp.651-657
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• 1993

The protective effects of dietary vatamin E and selenium on peroxidative damage and hematopoietic inhibition by lead poisoning were investigated in rats. Male Sprague-Dawley rats weighing 150$\pm$5g were divided into six groups according to dietary vitamin E and / or selenium levels, i.e. control(vitamin E, 40mg/kg diet), 0E(without vitamin E, Se), 40E(vitamin E, 40mg/kg diet ; without Se), 200E(vitamin E, 200mg/kg diet ; without Se), 200ES(vitamin E, 200mg/kg diet ; Se, 0.5ppm) and 0Es(without vitamin E ; Se, 0.5ppm) groups. All experimental groups were fed ad libitum 2000ppm lead in diet except control for 4 weeks. Hemoglobin contents and hematocrit values of lead groups were lower than control group except 200ES group and were the lowest in 0E group. Aminolevulinic acid dehydratase(ALAD) activities of blood and liver were sequentially reduced in 200ES, 200E, 0ES, 40E and 0E groups, compared to control, were as urinary aminolevulinic acid (ALA) excretions were increased in the groups which represented low ALAD activity. Heapatic superoxide dismutase(SOD) activities was lower in 0E, and higher in 40E, 200E and 200ES groups, compared with control. Glutathione peroxidase(GPX) activities of liver were reduced in 0E and 40E groups, but those of 0ES, 200E and 200ES groups were significantly increased. Especially GPX activities in 200ES and 200ES groups were not different from control group. The reduced glutathione contents in liver were lowest in 0E and 40E groups, compared with control, whereas levels of the oxidized form were opposite phenomena of that. Liver lipid peroxide values of 0E, 0ES, 40E and 200E groups were 6.4, 2.9, 2.1 and 1.3 fold higher than control, respectively, but 200ES groups was not different from control.

• The Korea Journal of Herbology
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• v.39 no.1
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• pp.31-38
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• 2024

Objectives : Ulcerative colitis is a chronic recurrent inflammatory disease of the gastrointestinal tract. However, there are some drawbacks to long-term drug therapy such as the risk of opportunistic infections. Recently, there was an increasing interest on the use of khorasan Kamut wheat because of their higher value of selenium and fiber than modern wheat. The present study was aimed to investigate the effect of Kamut brand wheat enzyme (Kamut WE) diet on colon health in dextran sulfate sodium (DSS)-induced colitis mice. Methods : Female C57BL/6J mice were divided into 6 groups. (1) normal (Water and AIN-93G diet), (2) control (1.25% DSS and AIN-93G diet), (3) Kamut WE (1.25% DSS and Kamut WE diet), (4) normal (Water and AIN-93G diet), (5) control (2.50% DSS and AIN-93G diet), (6) Kamut WE (2.50% DSS and Kamut WE diet). Dietary intake, body weight change, disease activity index (DAI), colon length and spleen weight were monitored. Results : Kamut WE group alleviated colitis symptom, including dietary intake loss, DAI (weight loss, loose stools, bleeding), colon length shortening and spleen swelling. Further, Kamut WE diets showed a significant effect against pathological damage by the increased colon length, decreased DAI and spleen weight in DSS 1.25% as well as DSS 2.50%. Conclusions : Our study provides evidence that Kamut WE diet increased colon length, decreased DAI and spleen weight in intestinal inflammation.

• Journal of Marine Bioscience and Biotechnology
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• v.13 no.2
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• pp.86-93
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• 2021

A high salt diet contributes to kidney damage by causing hypoxia and oxidative stress. Recently, an increase in dietary salt has been reported to induce an inflammatory phenotype in immune cells, further contributing to kidney damage. However, studies on the exact mechanism and role of a high salt diet on the inflammatory response in the kidneys are still insufficient. In this study, a cisplatin-induced acute kidney injury model using C57BL/6 mice was used to analyze the effect of salt intake on kidney injury. Results showed that high salt administration aggravated kidney edema in mice induced by treatment with cisplatin. Moreover, the indicators of kidney and liver function impairment were significantly increased in the group cotreated with high salt compared with that treated with cisplatin alone. Furthermore, the exacerbation of kidney damage by high salt administration was also associated with a decrease in the number of cells in the immune regulatory system. Additionally, high salt administration further decreased renal perfusion functions along with increased cisplatin-induced damage to proximal tubules. This was accompanied by increased expression of T cell immunoglobulin, mucin domain 1 (a biomarker of kidney injury), and Bax (a pro-apoptotic factor). Moreover, cisplatin-induced expression of proinflammatory mediators and cytokines, including cyclooxygenase-2 and tumor necrosis factor-α in kidney tissue, was further increased by high salt intake. Therefore, these results indicate that the kidney's inflammatory response by high salt treatment can further promote kidney damage caused by various pathological factors.