Chinese Journal of Pharmacovigilance ›› 2016, Vol. 13 ›› Issue (7): 385-388.

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Protective Effect of Bicyclol on Glucosides of Tripterygium Wilfordii-induced Liver Injury in Mice

LIU Ning, ZHANG You-wen, ZHANG Dan, BAO Xiu-qi, SUN Hua   

  1. State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China
  • Received:2016-06-21 Revised:2018-07-17 Online:2016-07-20 Published:2018-07-17

Abstract: Objective To study the protective effect of bicyclol on glucosides of Tripterygium wilfordii-induced liver injury in ICR mice. Methods ICR mice were given intragastric administration bicyclol (50, 100, 200 mg·kg-1) for three times. Two hours after the last administration, the mice were treated with glucosides of Tripterygium wilfordii 300 mg·kg-1 to establish the liver damage model. All animals were killed on 18 h after glucosides of Tripterygium wilfordii treatment. The activities of ALT, AST and LDH in serum were measured by automatic chemistry analyzer. Liver histopathological changes were examined by H.E. and light microscopy. Western blot was carried out to analyze the protein level of liver. Results Glucosides of Tripterygium wilfordii 300 mg·kg-1 could induce significant toxicity and liver damage, the mortality rate of mice was 41.67%. The levels of serum ALT, AST, LDH significantly increased and there were hepatocyte apoptosis and inflammatory cell infiltration in liver tissue. 50, 100, 200 mg·kg-1 bicyclol could reduce the mortality rate of mice and the blood biochemical indexes, including ALT, AST and LDH. The results of H.E. staining showed that bicyclol could prevent the steatosis of liver and colliquative necrosis of liver cells. The results of Western blot showed that bicyclol could simulate PI3K pathway, decrease the expression of Fas L, and increase the expression of connexin-43. Conclusion Bicyclol showed a significant protective effect on glucosides of Tripterygium wilfordii -induced liver injury in mice. This may be in connection with inhibiting apoptosis and recovering the gap junctions intercellular communication.

Key words: glucosides of Tripterygium wilfordii, bicyclol, DILI, gap junction

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