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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2007.3
- 수록면
- 95 - 101 (7page)
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The hepato-protective activity of the lipoic acid complex (LAC) has been studied in the rats against carbon tetrachloride (CCI₄)-ethanol-induced liver toxicity. Rats were fed 10% ethanol in drinking water for 8 weeks. From 1 week after the start of ethanol feeding, the animals were subcutaneously treated with single dose of 1 ㎖/㎏ CCI₄ (2 ㎖/㎏ as 50% in corn oil), and one week later, followed by 0.5 ㎖/㎏ CCI₄ twice per week for 7 weeks. After 8-week induction of liver dysfunction, the rats were orally administered with LAC (200 or 800 ㎎/㎏) or silymarin (80 ㎎/㎏), or their vehicle (0.5% carboxymethyl cellulose, CMC) for 4 weeks, along with additional 4-week treatment of ethanol and CCI₄ (0.5 ㎎/㎏). CCI₄ induced hepatocellular degeneration and necrosis, leading to a great increase in serum aspartate aminotransferase (AST) and alanine aminotrasferase (ALT). Also, lipid peroxidation and fibrosis of liver tissues were confirmed by malondialdehyde (MDA) and hydroxyproline. In addition to AST and ALT, increased TSARS and hydroxyproline contents caused by CCI₄ were significantly attenuated by LAC in a dose-dependent manner. In histopathological results, severe vacoulations and inflammatory cell infiltrations around portal triad were observed in CCI₄-treated rats, which were greatly attenuated by LAC treatment. These results support the effectiveness of LAC for the treatment of hepatic fibrosis.
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