• Journal of Nutrition and Health
• /
• v.37 no.3
• /
• pp.169-175
• /
• 2004

This study was performed to investigate the effect of acorn supplementation on the lipid profile and redox antioxidant enzyme activities in obese rat. Obesity in the rats was induced by feeding diet contained 10％ lard and 0.5％ cholesterol for 4 week. After 4 weeks, rats were divided into the following 5 groups; high fat diet (Control), high fat diet plus 10％ Acorn powder (APlO％), high fat diet plus 20％ Acorn powder (AP20％), high fat diet plus 0.2％ Acorn extract (AE0.2％), high fat diet plus 0.5％ Acorn extract (AE0.5％). Total food intake and food efficiency ratio (FER) was not significantly different by acorn powder and extract supplementation. But, body weight was decreased by 20％ acorn powder. Acorn powder and extract supplementation for 4 weeks tend to decrease total cholesterol and triglyceride level on the serum and hepatic tissue. There was no significant difference in hepatic glutathione (GSH) content among all the groups. The hepatic GST activity in acorn supplemented groups was lower than that of control. Glutathione peroxidase and catalase activities were higher in acorn supplemented groups than that of control. Hepatic TBARS levels of experimental groups were also significantly lower than that of control group. Our finding suggest that acorn powders and extract might have potential role for improving lipid profiles and antioxidant enzyme activities in obese rats.

• Journal of Nutrition and Health
• /
• v.41 no.4
• /
• pp.299-306
• /
• 2008

The purpose of this research was to investigate the effect of the calcium intake on lipid profile and antioxidant capacities in ovariectomized (OVX) rats. Rats were divided into 3 groups and fed diet with different levels of calcium (low 0.1%, adequate 0.5%, high 1.5%) for 4 weeks. The half of rats in each group was ovariectomized and the others were sham-operated. And rats were fed same diets for 8 weeks after operation. Feed intake and weight gain were significantly higher in OVX group than those in sham-operated. Serum HDL-cholesterol was the highest in high-calcium group of OVX. Hepatic triglyceride of low-calcium group in sham-operated was the highest, while that of highcalcium group in OVX was the highest. Hepatic activities of glutathione-S-transferase (GST), glutathione peroxidase (GSH-Px), and catalase were significantly decreased by increasement of calcium intake. Hepatic TBARS level was the lowest in high-calcium group of OVX. And hepatic level of TBARS induced by AAPH was significantly decreased by increasement of calcium intake. These results may indicate that the high calcium intake have the potential role to improve lipid profiles and antioxidant capacities in OVX rats.

• Journal of Yeungnam Medical Science
• /
• v.35 no.1
• /
• pp.127-129
• /
• 2018

Fitz-Hugh-Curtis syndrome (FHCS) is characterized by inflammation of the perihepatic capsules associated with the pelvic inflammatory disease (PID). FHCS is not a serious disease, but if not treated properly, it can result in increased medical costs, prolonged treatment, and dissatisfaction with treatment. However, early recognition of FHCS in the emergency department can be difficult because its symptoms or physical findings may mimic many other diseases. Although contrast-enhanced computed tomography (CECT) is the useful imaging modality for recognition of FHCS, it is available only when a high suspicion is established. We performed point-of-care ultrasonography in an 18-year-old woman who had a sharp right upper quadrant (RUQ) abdominal pain without PID symptoms and found a thickened or three-layer hepatic capsule. These findings coincided with areas showing increased hepatic capsular enhancement in the arterial phase of CECT. These results show that if the thickened or three-layer hepatic capsule without evidence of a common cause of RUQ pain is observed on ultrasonography in women of childbearing age with RUQ abdominal pain, the physician can consider the possibility of FHCS.

• Archives of Pharmacal Research
• /
• v.25 no.4
• /
• pp.397-415
• /
• 2002

This paper deals with a crucial mechanism for interaction of basic drugs and cardiac glycosides at the hepatic uptake level. Available literature data is provided and new material is presented to picture the differential transport inhibition of bulky (type2) cationic drugs by a number of cardiac glycosides in rat liver. It is shown that the so called organic anion transporting peptide 2 (oatp2) is the likely interaction site: differential inhibition patterns as observed in oocytes expressing oatp2, could be clearly identified also in isolated rat hepatocytes, isolated perfused rat liver and the rat in vivo. The anticipation of transport interactions at the hepatic clearance level should be based on data on the relative affinities of interacting substrates for the transport systems involved along with knowledge on the pharmacokinetics of these agents as well as the chosen dose regimen in the studied species. This review highlights the importance of multispecific tranporter systems such as OATP, accommodating a broad spectrum of organic compounds of various charge, implying potential transport interactions that can affect body distribution and organ clearance.

• Archives of Pharmacal Research
• /
• v.28 no.12
• /
• pp.1392-1399
• /
• 2005

This study evaluated the effect of $\alpha$-tocopherol ($\alpha$-TC), ischemic preconditioning (IPC) or a combination on the extent of mitochondrial injury caused by hepatic ischemia/reperfusion (I/R). Rats were pretreated with $\alpha$-TC (20 mg/kg per day, i.p.) for 3 days before sustained ischemia. A rat liver was preconditioned with 10 min of ischemia and 10 min of reperfusion, and was then subjected to 90 min of ischemia followed by 5 h or 24 h of reperfusion. I/R increased the aminotransferase activity and mitochondrial lipid peroxidation, whereas it decreased the mitochondrial glutamate dehydrogenase activity. $\alpha$-TC and IPC individually attenuated these changes. $\alpha$-TC combined with IPC ($\alpha$-TC+IPC) did not further attenuate the changes. The mitochondrial glutathione content decreased after 5 h reperfusion. This decrease was attenuated by $\alpha$-TC, IPC, and $\alpha$-TC+IPC. The significant production of peroxides observed after 10 min reperfusion subsequent to sustained ischemia was attenuated by $\alpha$-TC, IPC, and $\alpha$-TC+IPC. The mitochondria isolated after I/R were rapidly swollen. However, this swelling rate was reduced by $\alpha$­TC, IPC, and $\alpha$-TC+IPC. These results suggest that either $\alpha$-TC or IPC reduces the level of mitochondrial damage associated with oxidative stress caused by hepatic I/R, but $\alpha$- TC combined with IPC offers no significant additional protection.

• Journal of radiological science and technology
• /
• v.42 no.3
• /
• pp.187-194
• /
• 2019

The purpose of this study was to evaluate the pathologic results of hepatic parenchyma parameters such as liver parenchyma, liver surface, liver margin and liver, portal vein, spleen size, And to evaluate the usefulness of fibrosis progression and hepatic ultrasonography. The sensitivity, specificity, positive predictive value, and prognostic value according to the stage of fibrosis and grade of inflammation were divided into two groups according to the morphologic variable "A" through ultrasound and "B" We evaluated the predictive value and predicted the variables to evaluate fibrosis in clinical diagnosis and treatment of patients with chronic liver disease. The sensitivity and specificity of hepatic fibrosis in hepatic morphologic variables and other size variables were highest in liver surface and edge. The morphologic parameters used in the evaluation of fibrosis were clinically relevant in distinguishing the fibrosis stage from the results of liver biopsy.

• The Korean Journal of Physiology and Pharmacology
• /
• v.23 no.4
• /
• pp.263-270
• /
• 2019

Hydrogen sulfide is well-known to exhibit anti-inflammatory and cytoprotective activities, and also has protective effects in the liver. This study aimed to examine the protective effect of hydrogen sulfide in rats with hepatic encephalopathy, which was induced by mild bile duct ligation. In this rat model, bile ducts were mildly ligated for 26 days. Rats were treated for the final 5 days with sodium hydrosulfide (NaHS). NaHS ($25{\mu}mol/kg$), 0.5% sodium carboxymethyl cellulose, or silymarin (100 mg/kg) was administered intraperitoneally once per day for 5 consecutive days. Mild bile duct ligation caused hepatotoxicity and inflammation in rats. Intraperitoneal NaHS administration reduced levels of aspartate aminotransferase and alanine aminotransferase, which are indicators of liver disease, compared to levels in the control mild bile duct ligation group. Levels of ammonia, a major causative factor of hepatic encephalopathy, were also significantly decreased. Malondialdehyde, myeloperoxidase, catalase, and tumor necrosis factor-${\alpha}$ levels were measured to confirm antioxidative and anti-inflammatory effects. N-Methyl-D-aspartic acid (NMDA) receptors with neurotoxic activity were assessed for subunit NMDA receptor subtype 2B. Based on these data, NaHS is suggested to exhibit hepatoprotective effects and guard against neurotoxicity through antioxidant and anti-inflammatory actions.

• Molecules and Cells
• /
• v.44 no.2
• /
• pp.116-125
• /
• 2021

Cardiovascular diseases (CVDs) are the most common cause of death in patients with nonalcoholic fatty liver disease (NAFLD) and dyslipidemia is considered at least partially responsible for the increased CVD risk in NAFLD patients. The aim of the present study is to understand how hepatic de novo lipogenesis influences hepatic cholesterol content as well as its effects on the plasma lipid levels. Hepatic lipogenesis was induced in mice by feeding a fat-free/high-sucrose (FF/HS) diet and the metabolic pathways associated with cholesterol were then analyzed. Both liver triglyceride and cholesterol contents were significantly increased in mice fed an FF/HS diet. Activation of fatty acid synthesis driven by the activation of sterol regulatory element binding protein (SREBP)-1c resulted in the increased liver triglycerides. The augmented cholesterol content in the liver could not be explained by an increased cholesterol synthesis, which was decreased by the FF/HS diet. HMG-CoA reductase protein level was decreased in mice fed an FF/HS diet. We found that the liver retained more cholesterol through a reduced excretion of bile acids, a reduced fecal cholesterol excretion, and an increased cholesterol uptake from plasma lipoproteins. Very low-density lipoproteintriglyceride and -cholesterol secretion were increased in mice fed an FF/HS diet, which led to hypertriglyceridemia and hypercholesterolemia in Ldlr-/- mice, a model that exhibits a more human like lipoprotein profile. These findings suggest that dietary cholesterol intake and cholesterol synthesis rates cannot only explain the hypercholesterolemia associated with NAFLD, and that the control of fatty acid synthesis should be considered for the management of dyslipidemia.

• Animal Bioscience
• /
• v.35 no.6
• /
• pp.938-947
• /
• 2022

Objective: The beneficial effects of glycine were tested in piglets with diquat-induced hepatic injury. Methods: Thirty-two piglets were assigned by a 2×2 factorial experimental design including glycine supplementation and diquat challenge. After 3 weeks of feeding with a basic diet or a 1% glycine supplemented diet, piglets were challenged with diquat or saline. After 1 week later, the piglets were slaughtered and samples were collected. Results: Our results indicated that glycine alleviated diquat induced morphological hepatic injury, decreased the activities of plasma alanine aminotransferase, aspartate aminotransferase and glutamyl transpeptidase in the piglets under diquat challenge, and increased total antioxidant capacity and antioxidative enzyme activity significantly. Adding glycine enhanced the concentrations of hepatic adenosine triphosphate and adenosine diphosphate. Transmission electron microscope observation showed that diquat induced clear hepatocytes ferroptosis and its effect could be alleviated by glycine to a certain degree. Moreover, glycine significantly affected mRNA and protein expression of ferroptosis-related signals in the liver. Conclusion: These results demonstrated that glycine attenuated liver damage via inhibiting ferroptosis.

• Biomolecules & Therapeutics
• /
• v.30 no.5
• /
• pp.391-398
• /
• 2022

Polyploidization is a process by which cells are induced to possess more than two sets of chromosomes. Although polyploidization is not frequent in mammals, it is closely associated with development and differentiation of specific tissues and organs. The liver is one of the mammalian organs that displays ploidy dynamics in physiological homeostasis during its development. The ratio of polyploid hepatocytes increases significantly in response to hepatic injury from aging, viral infection, iron overload, surgical resection, or metabolic overload, such as that from non-alcoholic fatty liver diseases (NAFLDs). One of the unique features of NAFLD is the marked heterogeneity of hepatocyte nuclear size, which is strongly associated with an adverse liver-related outcome, such as hepatocellular carcinoma, liver transplantation, and liver-related death. Thus, hepatic polyploidization has been suggested as a potential driver in the progression of NAFLDs that are involved in the control of the multiple pathogenicity of the diseases. However, the importance of polyploidy in diverse pathophysiological contexts remains elusive. Recently, several studies reported successful improvement of symptoms of NAFLDs by reducing pathological polyploidy or by controlling cell cycle progression in animal models, suggesting that better understanding the mechanisms of pathological hepatic polyploidy may provide insights into the treatment of hepatic disorders.