2. Academic Validation
  3. Diosbulbin B-induced liver injury in mice and its mechanism

Diosbulbin B-induced liver injury in mice and its mechanism

  • Hum Exp Toxicol. 2014 Jul;33(7):729-36. doi: 10.1177/0960327113506232.
Yibo Ma 1,  Chengwei Niu 2,  Junming Wang 3,  Lili Ji 4,  Zhengtao Wang 1
Affiliations

Affiliations

  • 1 The MOE Key Laboratory for Standardization of Chinese Medicines and The Shanghai Key Laboratory for Compound Chinese medicines, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai, China Department of Pharmacognosy, China Pharmaceutical University, Nanjing, China.
  • 2 The MOE Key Laboratory for Standardization of Chinese Medicines and The Shanghai Key Laboratory for Compound Chinese medicines, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
  • 3 School of Pharmacy, Henan University of Traditional Chinese Medicine, Zhengzhou, China.
  • 4 The MOE Key Laboratory for Standardization of Chinese Medicines and The Shanghai Key Laboratory for Compound Chinese medicines, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai, China [email protected].
PMID: 24107456 DOI: 10.1177/0960327113506232
Abstract

Dioscorea bulbifera L., a commonly used medicinal plant in China, is reported to induce hepatotoxicity. The present study is undertaken to investigate the hepatotoxicity induced by diosbulbin B (DB), a diterpene lactone isolated from D. bulbifera L., and to further explore its underlying mechanism. DB was administered to mice at the doses of 0, 16, 32, and 64 mg/kg once daily for 12 consecutive days. Liver injury induced by DB was evidenced by the increased activity of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and Alkaline Phosphatase (ALP). Liver histological evaluation showed that the mice treated with DB exhibited liver damage with the swelling of hepatocytes. Further results showed that the amount of malondialdehyde (MDA) in the liver was increased in mice treated with DB, while the glutathione amount and the enzymatic activity of Glutathione Peroxidase (GPx), glutathione-S-transferase (GST), copper/zinc-superoxide dismutase (CuZn-SOD), manganese-SOD (Mn-SOD), and catalase (CAT) were all decreased. DB also decreased the gene expression of CuZn-SOD and CAT. Taken together, our results indicate that oral administration of DB for 12 consecutive days can lead to the oxidative stress liver injury in mice.

Keywords

Dioscorea bulbifera L.; diosbulbin B; hepatotoxicity; oxidative stress.

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