• Archives of Pharmacal Research
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• v.18 no.4
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• pp.289-292
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• 1995

Icariside II, a flavonol glycoside, was isolated from the aerial part of Epimedium Koreanum Nakai by the anti-hepatotoxic acitivity guided fractionation technique employing $CCl_4-in-toxicated$ primary cultured rat hepatocytes as an assay system. Its anti-hepatotoxic activity was evaluated by measuring activity of glutamic pyruvic transaminase released from the $CCl_4-in-toxicated$ primary cultured rat hapatocytes. Icariside II significantly reduced the activity of glutamic pyruvic transaminase released from the $CCl_4-in-toxicated$ primary cultured rat hepatocytes and resulted in 78% recovery of the toxicity at the concentration of $200{\;}\mu\textrm{m}$. The anti-hepatotoxic activity of icariside II on the $CCl_4-in-toxicated$ primary cultured rat hepatocytes was as potent as that of silybin.

• Advances in Traditional Medicine
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• v.4 no.1
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• pp.44-48
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• 2004

The Hexane Extract (HE) and Ethyl Acetate Soluble Fraction of the Methanolic Extract (EASFME) of the fruit pulp of Momordica dioica Roxb. (Cucurbitaceae) was evaluated for its anti-hepatotoxic activity in rats. Acute hepatotoxicity was induced by administering paracetamol (2 g/kg, p.o.) for 3 days. The extracts, at a dose of 400 mg/kg (p.o.) administered for 7 days exhibited a significant therapeutic effect by lowering Serum Glutamate Oxaloacetate Transaminase (SGOT), Serum Glutamate Pyruvate Transaminase (SGPT), Serum Alkaline Phosphatase (ALP) and Serum bilirubin and increasing the serum protein levels. These biochemical observations were supplemented by histopathological examination of the liver sections. The activity of extract was also comparable to the standard drug Silymarin, which is a well-known natural anti-hepatotoxic drug.

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2004.11a
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• pp.136-136
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• 2004

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2004.11a
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• pp.135-135
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• 2004

• The Journal of Korean Medicine
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• v.26 no.2 s.62
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• pp.152-165
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• 2005

Background: The use of herbal preparations as remedies for various medical conditions has continuously increased in Korea Large proportions of Korean patients use herbal medicinal products, folk remedies, and food supplements. However, studies on the safety of herbal products arc conducted on a less than sufficient basis even in the countries like Korea where herbal medicine is being used extensively. Some of the reports on the safety of herbs were done by the doctors of western medicine but lack of knowledge and misclassification led to misunderstandings. Objecitves: This study aims to review the recent evidences on hepatotoxic events associated with the use of herbal medicinal products, folk remedy, and food supplements. In the process, this review will grasp trends in this field of studies and will direct further researches into the right direction. Methods: Systematic literature searches were performed on MedRic and MEDLIS in Korea. Screening and selection of the articles and the extraction of data were performed independently by two of authors. There were no restrictions regarding the published date. In order to avoid bias, the articles written by medical doctors, not by oriental doctors were selected. 43 journals were chosen for the review. Results: Analyzing the number of journals, studies on the drug-induced liver injury were increased after the year 2000. The proportion of herbal and folk remedy associated hepatotoxic injuries in all drug-induced liver injury was $21.0\%-30.0\%$. But criterion for herbal medicine is rather vague and limited objective data hindered objectiveness. Few of single medicinal herbs and combination preparations were associated with hepatotoxic injuries. But because of lack of objectivity, further researches must be conducted to yield more concrete results. Conclusions: yield more concrete results. Incidence figures are largely unknown, and in most cases a causal attribution is not established. The challenge for the future is to systematically research this area, educate all parties involved, and minimize patient risks.

• Molecular & Cellular Toxicology
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• v.1 no.4
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• pp.268-274
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• 2005

Bromobenzene (BB) is well known hepatotoxicant. Also, BB is an industrial solvent that arouses toxicity predominantly in the liver where it causes centrilobular necrosis. BB is subjected to Cytochrome P450 mediated epoxidation followed by either conjugation with glutathione, enzymatic hydrolysis or further oxidation. In this study, we focused on BB-induced gene expression at non-hepatotoxic dose. Mice were exposed to two levels of BB, sampled at 24 h, and hepatic gene expression levels were determined to evaluate dose dependent changes. When examining the toxic dose of BB treated group in other previous studies, genes related to heat shock protein, oxidative stress, and drug metabolism are expressed. Compared to these results, our study, in which non-toxic dose of BB was administrated, showed similar patterns as the toxic conditions above. The purpose of the study was to select genes that showed changes in relation to the differing dose through confirmation of the difference within transcriptomic boundaries, but those that are not detected by the existing classic toxicology tools in non-hepatotoxic dose.

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.18 no.2
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• pp.80-85
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• 2005

A female visited the Dept. of Oriental Ophthamology & Otolaryngology & Dermatology, Dong-eui University with Facial Nerve Palsy in Herpes Zoster Oticus. She had been taking ill with chronic hepatitis B and taking western medicine. We treated a patient with only Oriental Medicine.(the herbal medication and acupuncture etc). Because she was afraid of herbal medicine -induced hepatitis, went through an examination about LFT profile regularly. The symptom of Herpes Zoster Oticus was improved and there was no abnormality in LFT profile. Through this case, we thought that it is possible to treat the other disease of the patient with chronic hepatitis using herbal medication without hepatotoxic hepatitis. But for the safety of patient and doctor in several case, we need to accumulate objective data about the side effect of herbal medications inducing hepatotoxic hepatitis.

• Korean Journal of Pharmacognosy
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• v.27 no.2
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• pp.111-116
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• 1996

The components were isolated from the root of Astragalus membranaceus and their structures were characterized as 3,4-methylenedioxypyrrolealdehyde, $7-O-{\beta}-D-glucopyranosyl$ 7, 3'-dihydroxy-4'-methoxy isoflavone and a naphthalene derivative on the basis of spectral and physical methods. $7-O-{\beta}-D-glucopyranosyl$ 7, 3'-dihydroxy-4'-methoxy isoflavone and the naphthalene compound showed protective effect on $CC_{l4}-induced$ cytotoxicity in primary cultured rat hepatocytes.

• Toxicological Research
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• v.3 no.2
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• pp.129-141
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• 1987

Hepatocytes isolated from rats which have been pretreated with phenobarbital (80 mg/kg for 3 days), were able to take up N-acetylcysteine from surrounding medium and were able to synthesize the reduced glutathione ($GSH^{\ast}-3$) intracellularly. The N-acetylcysteine is quickly deacetylated after the uptake and increases the pool size of cysteine, which was very low initially (5 nmol/$10^6$ cells). From this increased intracellular cysteine pool, GSH was synthesized. Freshly isolated rat hepatocytes contained a high level of GSH (30 nmol/$10^6$ cells), but upon incubation with the diethylmaleate, it was markedly decreased (10 nmol/$10^6$ cells). The hepatocytes with depleted GSH have lost viability upon incubations with acetaminophen (5mM) and paraquat (2 mM). However, when the N-acetylcysteine (1 mM) was added to this incubation condition, these chemical induced hepatocellular necrosis were prevented for longer durations. This N-acetylcysteine dependent protective effect against the hepatotoxic chemicals was lost by adding methionine sulfoximine (10 mM), an inhibitor of GSH biosynthesis. Both the carbontetrachloride (5 mM) and chioroform (5 mM) added to the incubation medium caused rapid losses of GSH and cell viability, even without the prior depletion of cellular GSH. However, again, if the 1mM N-acetylcysteine was supplemented, the rates of losses of GSH and cell viability were retarded in both cases. Even though large amounts of the added N-acetylcysteine was present in the cell, N-acetylcysteine conjugate of acetaminophen was not formed. Instead, only large amounts of GSH conjugate of the drug was produced. Thus, it is concluded that the added N-acetylcysteine is taken up and utilized for resynthesis of GSH. In turn, this resynthesized GSH contributes to the protection against cytotoxicity inducible with hepatotoxic drugs.

• Toxicological Research
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• v.7 no.2
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• pp.113-128
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• 1991

Hepatotoxicity has many facets. Those to be discussed in this review include the mechanism for the hepatotoxic effects, nature of the injury, and animal models of hepatotoxicity suitable for the detection of chemical injury. Some therapeutic drugs used for treatment of hepatitis are also presented. In addition, as an important and serious problem in future, alternative toxicity testing is discussed.