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王涛, 周植星, 刘薇, 江振洲, 赵郭林, 尚靖, 张陆勇. 秋水仙碱对大鼠胆管结扎所致胆汁淤积模型肝损伤的影响[J]. 中国药科大学学报, 2014, 45(6): 715-719. DOI: 10.11665/j.issn.1000-5048.20140618
引用本文: 王涛, 周植星, 刘薇, 江振洲, 赵郭林, 尚靖, 张陆勇. 秋水仙碱对大鼠胆管结扎所致胆汁淤积模型肝损伤的影响[J]. 中国药科大学学报, 2014, 45(6): 715-719. DOI: 10.11665/j.issn.1000-5048.20140618
WANG Tao, ZHOU Zhixing, LIU Wei, JIANG Zhenzhou, ZHAO Guolin, SHANG Jing, ZHANG Luyong. Effects of colchicine on cholestatic liver injury in rats induced by bile duct ligation[J]. Journal of China Pharmaceutical University, 2014, 45(6): 715-719. DOI: 10.11665/j.issn.1000-5048.20140618
Citation: WANG Tao, ZHOU Zhixing, LIU Wei, JIANG Zhenzhou, ZHAO Guolin, SHANG Jing, ZHANG Luyong. Effects of colchicine on cholestatic liver injury in rats induced by bile duct ligation[J]. Journal of China Pharmaceutical University, 2014, 45(6): 715-719. DOI: 10.11665/j.issn.1000-5048.20140618

秋水仙碱对大鼠胆管结扎所致胆汁淤积模型肝损伤的影响

Effects of colchicine on cholestatic liver injury in rats induced by bile duct ligation

  • 摘要: 考察秋水仙碱对大鼠胆管结扎所致胆汁淤积模型肝损伤的干预作用。采用胆总管结扎建立大鼠胆汁淤积模型,模型动物分别灌胃秋水仙碱0.12和0.24 mg/kg,连续7 d。通过血清生化指标、肝脏髓过氧化物酶(MPO)活力及肝脏组织病理学检查来评价秋水仙碱的作用。结果显示,秋水仙碱可显著降低模型动物血清ALP、γ-GTP、TBA水平。秋水仙碱高、低剂量组对肝脏MPO活力均有显著抑制作用,同时可明显改善肝脏的组织病理学改变。实验结果表明,小剂量的秋水仙碱(≤0.24 mg/kg)对于大鼠胆管结扎所致的胆管损伤具有明显的改善作用,而抑制炎性细胞活化和浸润可能是其重要的作用机制。

     

    Abstract: To investigate the effects of colchicine on the cholestasis in rats induced by bile duct ligation(BDL), colchicine(0. 12 and 0. 24 mg/kg)was administered intragastrically for 7 consecutive days after ligation of common bile duct. The effect of colchicines on the liver injury was evaluated by serum biochemistry(ALT, AST, ALP, γ-GTP, TBIL, DBIL, ALB and TBA), liver myeloperoxidase(MPO)activity as well as histological examination. Both doses of colchicine significantly decreased serum ALP, γ-GTP and TBA levels, inhibited liver MPO activity and alleviate liver histological changes, such as inflammatory cell infiltration and interlobular bile duct hyperplasia. Data suggested that lower dose of colchicines(≤0. 24 mg/kg)exerted protection of bile duct injury induced by BDL in rats involving primary mechanism on inhibiting activation and infiltration of inflammatory cells.

     

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