• Archives of Pharmacal Research
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• v.21 no.3
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• pp.236-240
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• 1998

The effect of thyroid hormones on the hepatic xanthine oxidase activity was studied in rats after the intraperitoneal injections of comthyroid (triiodotyronine:thyroxine=1:4) at 0.3 mg/kg for 3 consecutive days. The aim of this study was to understand the precise mechanism of hyperthyroidism induced by oxidative stress. The concentration of lipid peroxides determined indirectly by the measurement of thiobarbituric acid reactants was increased in comthyroid treated rats. The hepatic glutathione content was decreased in comthyroid injected rat compared to the euthyroid state. It was also observed that the increment of xanthine oxidase activity has a profound role in oxygen radicals generation system in comthyroid treated rat. These findings suggest that the enhanced xanthine oxidase activity and depleting glutathione content in comthyroid treated rats result in pathophysiological oxidative stress including an increment of hepatic lipid peroxidation.

• Natural Product Sciences
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• v.8 no.1
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• pp.18-22
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• 2002

Inhibitory effects of the essential oils obtained from ten herbs were tested on acetaminophen-induced lipid peroxidation in the rat. The oil of Artemisia princeps var. orientalis buds (AP-oil) showed the most significant hepatic malondialdehyde value which was comparable to those of ascorbic acid and methionine. This was warranted by the protective effect on hepatic glutathione depletion. Overview of the data on the activities of hepatic microsomal enzymes, aminopyrine N-demethylase and aniline hydroxylase led to the notice that the suppressed activities of those enzymes are mainly responsible for the anti-lipid peroxidation. The interpretation of GC-MS data on the AP-oil revealed the ingredient of cineol, thujone, carvone, borneol, camphor and terpineol.

• Natural Product Sciences
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• v.19 no.3
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• pp.231-235
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• 2013

Activity-guided isolation to search for antifibrotic compounds from natural products using HSC-T6 cells afforded nine flavonoids or phenolics, luteolin (1), 3'-O-methylorobol (2), acactin 7-rutinoside (3), sedelolactone (4), 4-methoxyphenol (5), 4-hydroxyaldehyde (6), 4-hydoxyaldehyde (7), 4-hydroxy-3-methoxybenzoic acid (8), and ferulic acid (9) from the methanolic extract of aerial parts of Eclipta prostrata L.. Among the isolated compounds, luteolin (1) significantly inhibited the proliferation of HSCs in dose- and time-dependent manners. Antifibrotic activity of E. prostrata and its phenolic compounds might provide potential therapeutical choice in the treatment of hepatic fibrosis.

• Toxicological Research
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• v.23 no.4
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• pp.289-299
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• 2007

Lipopolysaccharide (LPS) endotoxin is an active component in the outer membrane of Gram-negative bacteria. LPS is usually used as an inflammatory animal model. During the inflammation, diarrhea and changes in plasma proteins, in hepatic and/or intestinal microsomal cytochrome P450 (CYP) isozymes, and in the renal and/or biliary excretion of drugs have been reported. Thus, in rats pretreated with lipopolysaccharide endotoxin isolated from Klebsiella pneumoniae (KPLPS rats), the absorption, distribution, metabolism, and excretion of drugs could be expected to be altered. Interestingly time-dependent effects on the hepatic CYP isozymes have been reported in KPLPS rats. Thus, in KPLPS rats, the pharmacokinetics of drugs which are mainly metabolized via CYP isozymes could be expected to be time-dependent. In this review, an attempt to explain changes in pharmacokinetics of drug reported in the literature was made in terms of CYP isozyme changes or urinary and/or biliary excretion changes in KPLPS rats.

• Korean Journal of Veterinary Research
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• v.19 no.1
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• pp.23-26
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• 1979

In order to compare the effects of epinephrine, cortisone or insulin on the hepatic storage of triglycerides, the fatty liver was induced in mice by the subcutaneous injection for 30 days of either epinephrine, cortisone or insulin. The morphological characteristics of fatty liver in relation to the inducing agents was observed with the following results. 1. The fatty liver induced by epinephrine or cortisone was characterized by the centrilobular accumulation of triglycerides although the degree of accumulation by epinephrine appeared to be much higher than that by cortisone. 2. The fatty liver produced by insulin, however, was characterized by the infiltration of small-sized lipid droplets scattering all over the hepatic lobules.

• Journal of Nutrition and Health
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• v.24 no.6
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• pp.485-495
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• 1991

Using isolated perfused livers obtained from rats that have been fed saturated and unsatu-rated fatty acid diets the rates of hepatic microsomal oxidation of 7-ethoxycoumarin(EC) to 7-hydroxycoumarin(HC) and the rates of subsequent conjugation of the produced HC to its glucuronide and sulfate esters have been determined. Prior to preparing the isolated perfused livers. rats were fed either fat free diet 10% beef tallow diet or 10% corn oil diet for 3 weeks. The rates of oxidation from EC to HC and also of the subsequent glucuronidation of HC were higher in the corn oil diet group than those found for the fat free and beef tallow diet groups. When the concentrations of infusing EC were increased stepwise there was a dose-dependnet increase for the release of the glucuronide form of HC metabolites at the expense of the sulfate ester form. This dose dependant shift observed for the corn oil group was more significnat than those found for other groups. These results indicate that corn oil feeding has produced enhancement in the rates of hepatic microsomal drug oxidation and glucuronide conjugation the reactions catalyzed by enzymes embedded in the hepatic microsomal membranes.

• Journal of Nutrition and Health
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• v.37 no.5
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• pp.347-351
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• 2004

This study was carried out to investigate the supplementary effects of ${\gamma}$-oryzanol extracted from rice bran on lipid metabolism in diabetic mice. We supplied 2 kinds of experimental diets (CO without and GO with 0.2％ ${\gamma}$-oryzanol) to diabetic mice for 8 weeks. Diet intake, body weight, organ weight, contents of serum and hepatic lipid profiles, and fecal lipid levels were measured. Though there was no significant difference in diet intake, body weight change and organ weight between experimental groups, the concentration of serum total cholesterol and hepatic total lipid, total cholesterol and HMG-CoA reductase activity was significantly lower in GO group treated with 0.2％ ${\gamma}$-oryzanol of diet than CO group after supplementary period of experimental diets. And total lipid, triglyceride, total cholesterol, and bile acid levels excreted to feces were significantly higher in GO group than CO group. These results suggest that ${\gamma}$-oryzanol decrease the serum and hepatic lipid levels by lowing HMG-CoA reductase activity or increasing the contents of fecal lipid in diabetic KK mice.

• Biomedical Science Letters
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• v.9 no.1
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• pp.21-27
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• 2003

Hepatic subcellular $\alpha$-D-mannosidases activities and its Km and Vmax values were determined in chronic ethanol intoxicated rats with extrahepatic cholestasis induced by common bile duct ligation to manifest the biochemical background of alcohol drinking hazard under the hepatobiliary disease. In case of extrahepatic cholestasis, chronic ethanol intoxication in animals led to the increased activities of liver Golgi and microsomal $\alpha$-D-mannosidase as well as the Vmax values of these enzymes. However, the difference of Km values on hepatic subcellular enzymes were not found between the experimental groups. Therefore, the results indicate that the liver Golgi and microsomal $\alpha$-D-mannosidase may be more induced in chronic ethanol intoxication animals in case of cholestasis. Accordingly, the resulting data supported the fact that alcoholic drinks may led to enhancement of the hepatobiliary liver damage.

• The Korean Journal of Physiology and Pharmacology
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• v.4 no.2
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• pp.121-127
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• 2000

Intracellular accumulation of bile acids in the hepatocytes during cholestasis is thought to be pathogenic in cholestatic liver diseases. The objective of this study was to determine the role of lipid peroxidation and glutathione on the bile acid-induced hepatic cell death mechanism in primary cultured rat hepatocytes. To induce hepatic cell death, we incubated primary cultured rat hepatocytes with glycochenodeoxycholic acid $(GCDC;\;0{\sim}400\;{\mu}M)$ for 3 hours. In electron microscopic examination and agarose gel electrophoresis, low concentration of GCDC treatment mainly induced apoptotic feature. Whereas $400\;{\mu}M$ GCDC treated cells demonstrated both apoptosis and necrosis. Lipid peroxidation was increased dose-dependently in GCDC treated hepatocyte. And this was also accompanied by decreased glutathione. Therefore, oxygen free radical damage may play a partial role in GCDC-induced hepatic cell death.

• Korean Journal of Veterinary Research
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• v.36 no.3
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• pp.565-570
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• 1996

Cardiac, hepatic and renal mitochondria in rats fed lead containing diets were isolated and their activities were studied in terms of NADH oxidation. In normal rats, cardiac and renal mitochondria had similar activities and showed activity values of higher than those in hepatic mitochondria. Cardiac mitochondiral activities in rats fed lead containing diets were increased after 4 weeks of feeding but decreased to activity values close to normal. Renal mitochondrial activities showed a trend of inhibition in all groups fed lead containing diets but were no differenes by feeding periods of 4 and 8 weeks. Feeding of lead containing diets could not be attributed to any changes in the hepatic mitochondrial antivities at experimental doses during 4~8 weeks.