• Toxicological Research
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• 제2권1호
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• pp.31-36
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• 1986

The present work was undertaken to investigate the effect of glycyrrhetinic acid on pyridine toxicity. When glycyrrhetinic acid was pretreated, pyridine-induced CNS depression and mortality were decreased. A striking enhancement of serum transaminase activities after pyridine administration was markedly decreased by glycyrrhetinic acid pretreatment. It was also observed that the hepatic microsomal aniline hydroxylase activity, which is concerned with pyridine metabolism, was significantly increased in glycyrrhetinic acid pretreated mice.

• BMB Reports
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• 제40권6호
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• pp.1039-1049
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• 2007

Overdoses of acetaminophen cause hepato-renal oxidative stress. The present study was undertaken to investigate the protective effect of a 43 kDa protein isolated from the herb Cajanus indicus, against acetaminophen-induced hepatic and renal toxicity. Male albino mice were treated with the protein for 4 days (intraperitoneally, 2 mg/kg body wt) prior or post to oral administration of acetaminophen (300 mg/kg body wt) for 2 days. Levels of different marker enzymes (namely, glutamate pyruvate transaminase and alkaline phosphatase), creatinine and blood urea nitrogen were measured in the experimental sera. Intracellular reactive oxygen species production and total antioxidant activity were also determined from acetaminophen and protein treated hepatocytes. Indices of different antioxidant enzymes (namely, superoxide dismutase, catalase, glutathione-S-transferase) as well as lipid peroxidation end-products and glutathione were determined in both liver and kidney homogenates. In addition, Cytochrome P450 activity was also measured from liver microsomes. Finally, histopathological studies were performed from liver sections of control, acetaminophen-treated and protein pre- and post-treated (along with acetaminophen) mice. Administration of acetaminophen increased all the serum markers and creatinine levels in mice sera along with the enhancement of hepatic and renal lipid peroxidation. Besides, application of acetaminophen to hepatocytes increased reactive oxygen species production and reduced the total antioxidant activity of the treated hepatocytes. It also reduced the levels of antioxidant enzymes and cellular reserves of glutathione in liver and kidney. In addition, acetaminophen enhanced the cytochrome P450 activity of liver microsomes. Treatment with the protein significantly reversed these changes to almost normal. Apart from these, histopathological changes also revealed the protective nature of the protein against acetaminophen induced necrotic damage of the liver tissues. Results suggest that the protein protects hepatic and renal tissues against oxidative damages and could be used as an effective protector against acetaminophen induced hepato-nephrotoxicity.

• 동의생리병리학회지
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• 제24권2호
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• pp.249-257
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• 2010

Crataegii Fructus is commonly used as a improving digestion, removing retention of food, promoting blood circulation and resolving blood stasis agent in East Asia. Cadmium (Cd) is widely distributed in the environment due to its use in industry. An exposure to Cd causes dysuria, polyuria, chest pain, hepatic and renal tubular diseases. The liver is the most important target organ when considering Cd-induced toxicity because Cd primarily accumulates in the liver. This study investigated the protective effect of Crataegii Fructus water extract against cadmium ($CdCl_2$, Cd)-induced liver toxicity in H4IIE cells, a rat hepatocyte-derived cell line and in rats. Cell viability was significantly reduced in Cd-treated H4IIE cells in a time and concentration-dependent manner. However, Crataegii Fructus water extract (CFE) protected the cells from Cd-induced cytotoxicity via inhibition of PARP cleavage. To induce acute toxicity in rats, Cd (4 mg/kg body weight) was dissolved in normal saline and intravenously injected into rats. The rats then received either a vehicle or silymarin (as a positive control) or CFE (50, 100 mg/kg/day) for 3 days, and were subsequently exposed to a single injection of Cd. Alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) were significantly increased by Cd treatment. In contrast, pretreatment with CFE reduced ALT, AST and LDH. In histopathological analysis, CFE reduced the hepatic degenerative regions and the number of degenerative hepatocytes. These are considered as direct evidences that Crataegii Fructus has favorable inhibitory effects on the Cd-intoxicated liver damages. The efficacy of Crataegii Fructus shows slight lower than that of silymarin in the present study.

• 생약학회지
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• 제17권1호
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• pp.91-99
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• 1986

The single treatment of mice with steam distillate, non-volatile ether extract and methanol extract from mace (Arils of Myristica fragrans) caused a significant prolongation of hexobarbital-induced narcosis and increase in strychnine toxicity as well as a significant decrease in hepatic microsomal drug metabolizing enzyme activities. On 7 consecutive daily administrations, however, the duration of hypnosis was markedly shortened and significant increases in the hepatic enzyme activities were shown. With systematic fractionation by $SiO_2$ column chromatography of non-volatile ether fraction monitoring by animal tests a new lignan (mp $70{\sim}72^{\circ}$, MW 328, $[{\alpha}]^{20}_D+5.28$) was isolated as an active principle and its structure was elucidated as (2R, 3S)-1-(3,4-methylendioxyphenyl)-2,3 dimethyl-4-(4-hydroxy-3-methoxyphenyl) butane.

• Archives of Pharmacal Research
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• 제11권2호
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• pp.122-126
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• 1988

The effects of psoralen and angelicin on hepatic microsomal drug-metabolizing enzyme (DME) activities were investigated to elucidate the mode of the interaction of furanocoumarins with DME system. A single administration (30 mg/kg,i. p.) of both coumarins to mice cased a significant prolonagation of hexobarbital-induced hypnosis as well as an increase in strychnine toxicity. The inhibitory potencies of both coumarins as measured by rat hepatic microsomal aminopyrine N-demethylase and hexobarbital hydroxylase activities in vitro were considerably weaker than those of other furanocoumarins which possess a side chain moiety. Both coumarins were found to have significant inducing effects of DME system, with repeated treatments of them. The activities of an angular coumarin were stronger than those of a linear coumarin.

• 대한본초학회지
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• 제26권3호
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• pp.65-73
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• 2011

Objectives : The present study was evaluated the protective roles of Spatholobi Caulis in hepatotoxic rats due to APAP overdose. Methods : In experiments, rats were orally administrated with the aqueous extract of Spatholobi Caulis (SCE; 50, 100 mg/kg) for 4 days and then, orally gavage with APAP (1.2 g/kg) to induce acute liver damage. Results : Oral injection of APAP caused severe hepatic injury. Plasma ALT, AST and LDH levels were significantly elevated, but SCE significantly decreased ALT, AST and LDH to the normal level. In histopathological analysis, peripheral hemorrhage around portal triads and central necrosis around central veins were founded after APAP treatment. However, these histopathological changes were recovered by SCE pretreatment. SCE also decreased the percentage of generative hepatic regions (%/$mm^2$ hepatic parenchyma), the numbers of inflammatory cells (cells/$mm^2$ hepatic parenchyma) and the number of degenerative hepatic cells (N/100 hepatic cellls) which were significantly elevated after APAP injection. Furthermore, SCE down-regulated the contents of hepatic MDA and up-regulated hepatic GSH. SCE also inhibited the decrease in the expression of pro-caspase-3 by APAP treatment. Conclusions : Collectively, these data indicate that SCE protected APAP-induced hapatic damages through antioxidative and anti-apoptotic process. These findings the significant therapeutic potential of SCE during APAP-induced liver injury.

• 한국응용약물학회:학술대회논문집
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• 한국응용약물학회 2008년도 Proceedings of the Convention
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• pp.168-168
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• 2008

• 대한약학회:학술대회논문집
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• 대한약학회 2000년도 춘계총회 및 학술대회
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• pp.136.1-136.1
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• 2000

• 한방안이비인후피부과학회지
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• 제25권1호
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• pp.104-111
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• 2012

Objective : The aim of this study is to report the effect and safety of Traditional Korean Medicine on the treatment of erythrodermic psoriasis which appeared after stopping high potency topical steroids. Methods : A patient with psoriasis stopped topical steroids after the first outpatient care and was treated with herbal medicine, acupuncture, moxibustion for eight months. The severity of psoriasis was assessed with Psoriasis Area and Severity Index. Liver and renal functions were tested to observe the hepatic and renal toxicity of the treatment. Results : PASI score were 6.2 on the first visit and three months after it increased to 30 and the patient showed symptoms of erythrodermic psoriasis. And seven months after the first visit, it decreased to 0.6. There was no hepatic and renal toxicity of the treatment. Conclusion : These findings suggest that Traditional Korean Medicine might be effective and safe for the treatment of erythrodermic psoriasis.

• Molecular & Cellular Toxicology
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• 제4권2호
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• pp.138-143
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• 2008

We investigated if Chlorella vulgaris (CV) has protective effects on cadmium (Cd) induced liver damage in male Sprague-Dawley (SD) rats. Forty rats, aged 5 weeks old and weighed 90-110g, were divided into a control (with Cd free water), 50 ppm of $CdCl_2$ in drinking water treated groups (Chlorella 0% diet group (Cd/CV0%), Chlorella 5% diet group (Cd/CV5%) or Chlorella 10% diet group (Cd/CV10%). All the rats had freely access to water and diet for 8 weeks. The results show that body weight gain and relative liver weight had significantly lower in Cd/CV0%-treated group than in Cd/CV-treated groups. Hepatic Cd contents showed significantly less by feeding CV (P<0.05). Cd/CV0%-treated rats had significantly (P<0.05) higher hepatic T-MTs, and Cd-MTs concentrations, compared to Cd/CV5% or Cd/CV10% treated rats. The MT I/II mRNA was expressed in the liver of all experimental rats. Its expression was more increased in Cd/CV5%- or Cd/CV10%-treated rats, compared to control and Cd-treated rats. Thus, this study suggested that CV would have a protective effect on Cd-treated liver injury by the reduction of Cd concentrations and stimulation of Cd-MT binds in the liver. However, more studies are needed to identify the proper mechanism of CV and liver toxicity.