• Title/Summary/Keyword: Malloti cortex extract

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Effects of Malloti Cortex Water Extract, Bergenin, and Acetylbergenin on Liver Fibrosis Induced by Bile Duct Ligation in Rats

  • Chung, Myeon-Woo;Sunoo, Sub;Kim, Seung-Hwan;Kim, Hack-Seang
    • Biomolecules & Therapeutics
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    • v.9 no.2
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    • pp.112-118
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    • 2001
  • The effects of Malloti Cortex Water Extract (MCWE), bergenin (isolated as an active component from MCWE), and acetylbergenin (synthesized from acetylation of bergenin) on the liver fibrosis induced by bile duct ligation (BDL) in rats. We studied hydroxypro1ine (HYP) as a marker of collagen accumulation in the liver, alanine aminotransferase (s-ALT), aspartate aminotransferase (s-AST), and alkaline phosphatase (s-ALP) as serum markers of liver cell damage induced by BDL, MCWE, bergenin, and acetylbergenin decreased towards normal the accumulated levels of HYP in the liver and the elevated serum levels of s-ALT, s-AST and 5-ALP. The results indicate that MCWE, bergenin, and acetylbergenin ameliorated the liver damage induced by BDL in rats.

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Protective and Therapeutic Effects of Malloti Cortex Extract on Carbon Tetrachloride- and Galactosamine-induced Hepatotoxicity in Rats (예덕나무피엑스의 사염화탄소 및 갈락토사민 유발 간독성에 대한 보호 및 치료효과)

  • 임화경;김학성;최홍석;최종원
    • Biomolecules & Therapeutics
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    • v.7 no.1
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    • pp.35-43
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    • 1999
  • Hepatoprotective effects of Malloti cortex extract (MCE) from Mallotus japonicus against the carbon tetrachloride (CCl$_{4}$) and galactosamine (GalN) were investigated. Whereas serum aspartate aminotransferase and alanine aminotransferase levels were markedly elevated after CCl$_{4}$ and GalN administration, pretreatment and posttreatment with MCE before and after the injection of CCl$_{4}$ and GalN resulted in decreases in elevated serum aminotransferase activities. Whereas CCl$_{4}$ and GalN treatment caused 3~7 fold increases in sorbitol dehydrogenase and ${\gamma}$-glutamyltransferase activities, pretreatment and posttreatment with MCE resulted in the blocking of CCl$_{4}$ and GalN-induced liver toxicity. The hepatoprotective effect of MCE was in part due to MCE-induced elevation of hepatic glutathione levels. Pretreatment and posttreatment with MCE also reduced increased lipid peroxidation induced by CCl$_{4}$ and GalN. These results suggest that MCE may be useful for the prevention and therapy of hepatotoxic pathogenesis. It is presumed that protective and therapeutic effects of MCE due to be inducible glutathione S-transferase and glutathione reductase activities, involving in glutathione-medicated detoxication and maintainment of glutathione content, respectively.

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