Protection of a New Heptapeptide from Carapax trionycis against Carbon Tetrachloride-Induced Acute Liver Injury in Mice

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  • Wang Penglong
    School of Chinese Pharmacy, Beijing University of Chinese Medicine
  • Zhang Yuzhong
    Department of Pathology, Beijing University of Chinese Medicine
  • An Yawen
    School of Chinese Pharmacy, Beijing University of Chinese Medicine Institute of Materia Medica, Chinese Academy of Medical Sciences Peking Union Medical College
  • Xu Kuo
    School of Chinese Pharmacy, Beijing University of Chinese Medicine
  • Xu Xin
    School of Chinese Pharmacy, Beijing University of Chinese Medicine
  • Fu Chao
    School of Chinese Pharmacy, Beijing University of Chinese Medicine
  • Lin Jinxuan
    Department of Pathology, Beijing University of Chinese Medicine
  • Xu Shixun
    School of Chinese Pharmacy, Beijing University of Chinese Medicine
  • Li Qiang
    School of Chinese Pharmacy, Beijing University of Chinese Medicine
  • Lei Haimin
    School of Chinese Pharmacy, Beijing University of Chinese Medicine

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  • Protection of a New Heptapeptide from <i>Carapax trionycis</i> against Carbon Tetrachloride-Induced Acute Liver Injury in Mice

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A new heptapeptide GAGPHGG (OC1) was isolated from Carapax trionycis which was a traditional Chinese medicine (TCM) used for treatment of hepatic diseases. The structure of OC1 was characterized by MS, NMR techniques, together with amino acid sequence analysis. The hepatoprotective activity of OC1 was evaluated in vivo using the CCl4-induced acute liver injury model. Combining the pathological examination and the biochemical assays, OC1 (0.34 mg/kg, hypodermic injection) displayed better hepatoprotective effect than bifendate (100 mg/kg, intragastric administration) against the acute liver injury induced by carbon tetrachloride (CCl4) in mice. Compared with the model group, OC1 could significantly suppress the increase of serum level of aminotransferase (alanine transaminase (ALT) and aspartate aminotransferase (AST)), decrease the formation of malondialdehyde (MDA) and elevate the activity of glutathione peroxidase (GSH-Px) in liver (p<0.01). And the acute toxic test showed that median lethal dose (LD50) of OC1 exceeded 6.8 mg/kg, via hypodermic injection in mice.

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