Effects of Gomisin A on Liver Functions in Hepatotoxic Chemicals-Treated Rats

Maeda, Shinya; Takeda, Shogo; Miyamoto, Yoshimasa; Aburada, Masaki; Harada, Masatoshi

doi:10.1254/jjp.38.347

Cited by 29 publications

(16 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Gomisin A is the most active component among these lignans (20). It was reported that gomisin A prevents some experimental acute liver injuries (8). However, the nature of the protective mechanisms involved remains unclear.…”

Section: Discussionmentioning

confidence: 99%

“…Gomisin A improves histologically the hepatic cell degeneration, necrosis, and resultant inflammatory reactions in experimental liver injury models induced by carbon tetrachloride, GalN, α-naphthyl isothiocyanate, and orotonic acid (8). In addition, gomisin A has been reported to be effective in improving immunologicallyinduced acute hepatic failure (9) as well as in stimulating liver regeneration after a partial hepatectomy (10).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Anti-apoptotic and Hepatoprotective Effects of Gomisin A on Fulminant Hepatic Failure Induced by D-Galactosamine and Lipopolysaccharide in Mice

Kim

Kang

et al. 2008

J Pharmacol Sci

View full text Add to dashboard Cite

Abstract. This study examined the effects of gomisin A, a lignan compound from Schisandra fructus, on D-galactosamine (GalN) and lipopolysaccharide (LPS)-induced hepatic apoptosis and liver failure. Mice were given an intraperitoneal injection of GalN (700 mg /kg) / LPS (10 µg/ kg). Gomisin A (25, 50, 100, and 200 mg / kg) was administered intraperitoneally 1 h before the GalN / LPS injection. The liver injury was assessed biochemically and histologically. GalN/ LPS increased the serum aminotransferase levels and lipid peroxidation but decreased the reduced glutathione level. The pretreatment with gomisin A attenuated these changes in a dose-dependent manner. The survival rate of the gomisin A group was significantly higher than that of the control. The mitochondria isolated after the mice had been injected with GalN / LPS were swollen, which was attenuated by the gomisin A pretreatment. The elevation of serum tumor necrosis factor-α and activation of caspase-3 were observed in the GalN / LPS group, which was attenuated by gomisin A. The gomisin A-pretreated groups showed significantly fewer apoptotic (TUNEL-positive) cells and DNA fragmentation as compared with the GalN / LPS mice. The liver protection afforded by gomisin A is the result of the reduced oxidative stress and its antiapoptotic activity.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Anti-apoptotic and Hepatoprotective Effects of Gomisin A on Fulminant Hepatic Failure Induced by D-Galactosamine and Lipopolysaccharide in Mice

Kim

Kang

et al. 2008

J Pharmacol Sci

View full text Add to dashboard Cite

show abstract

“…Gomisin A suppressed the appear ance of the lesions in the early stages after 3'-MeDAB. It is possible that gomisin A de creases the reversible fractions by improving of hepatic functions (6)(7)(8). Other molecular mechanisms of inhibition by gomisin A of tumor promotion should be considered and in vestigations on these mechanisms are in prog ress in our laboratory.…”

Section: Discussionmentioning

confidence: 97%

Effects of Gomisin A on Hepatocarcinogenesis by 3’-Methyl-4-dimethylaminoazobenzene in Rats

Miyamoto

Wakusawa

Nomura

et al. 1991

Japanese Journal of Pharmacology

Self Cite

View full text Add to dashboard Cite

We examined the effects of gomisin A on tumor promotion in the liver after a short-term feeding of 3'-methyl-4-dimethylaminoazobenzene (3'-MeDAB) to rats, compared with the effects of phenobarbital. Male Donryu rats were fed ad libitum a diet containing 0.06% 3'-MeDAB and 0.03% or 0.01% gomisin A or water containing 0.05% phenobarbital. Gomisin A and phenobarbital did not cause any pro liferative and neoplastic lesions by themselves in 40 weeks of feeding. Altered foci in the liver increased with a peak at 12 weeks after the rats were fed 3'-MeDAB. Gomi sin A decreased the number of hepatic altered foci such as the clear cell and basophi lic cell type foci in the early stages. Phenobarbital enhanced neoplastic alterations so that the number and size of the foci were much larger in the phenobarbital-combined group than in the 3'-MeDAB-control group. Thus, phenobarbital acted as a promoter of cells initiated by 3'-MeDAB; on the other hand, gomisin A showed a weak sup pressive effect on tumor promotion.

show abstract

“…10 ) We investigated the effects of 1 on ICG clearance, and conclude that 1 accelerated the disappearance of plasma ICG in normal rats. This finding suggests that the process for hepatoprotection of 1 against both injuries may be related to an enhancement of the liver function, especially for hepatic transport.…”

Section: Mechanism For Antihepatotoxic Activitymentioning

confidence: 99%