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目的:以马兜铃酸A为剂量标准比较了关木通醇提物和关木通马兜铃总酸对小鼠的急性毒性,探讨关木通致毒的剂量关系。方法:小鼠单次灌胃关木通醇提物及其马兜铃总酸后,测定LD50、肝、肾功能及观察了肝、肾组织形态学变化。结果:小鼠给予关木通醇提物的LD50值为4.4g·kg-1,折合成马兜铃酸A为40mg·kg-1,与小鼠灌胃给予马兜铃总酸后的LD50值(折合成马兜铃酸A为♂33mg·kg-1,♀37mg·kg-1)相近。给予关木通醇提物剂量折合成马兜铃酸A为4.5mg·kg-1以上时,可引起血尿素氮和肌酐水平增高,同时可见肾脏组织形态学改变;折合成马兜铃酸A25mg·kg-1以上时可引起AST增高和肝脏组织形态学改变;以上病变程度均与马兜铃酸A的剂量成正比。结论:关木通除了有明显的肾脏毒性外,还有肝脏毒性,致肾毒剂量较致肝毒剂量低,肾脏毒性是关木通致死的主要原因,马兜铃酸是主要的致肾毒成分。关木通的致死和致肾毒作用与马兜铃酸A的剂量成正比例。
OBJECTIVE: To compare the acute toxicity of Guan Mu Tong alcohol extract and Guan Mu Tong Aristolochic acid in mice with aristolochic acid A as a dose standard, and to investigate the dose relationship of Guan Mu Tong toxicity. METHODS: After a single oral gavage of Aristolochia meniscus and total aristolochic acid in mice, the LD50, liver and kidney functions were measured, and the morphological changes of liver and kidney tissues were observed. RESULTS: The LD50 value of the ethanol extract of G. giraldii was 4.4 g·kg-1, and the aristolochic acid A was 40 mg·kg-1. The LD50 value of mice fed with aristolochic acid was gavage. The synthesis of aristolochic acid A was similar to ♂33mg·kg-1 and ♀37mg·kg-1). When the dose of aristolochic acid A was 4.5 mg·kg-1 or more, the levels of blood urea nitrogen and creatinine could be increased, and the morphological changes of the kidney could be seen. The aristolochic acid A25mg·kg Above -1, it can cause increased AST and liver tissue morphological changes; the above lesions are proportional to the dose of aristolochic acid A. Conclusion: In addition to obvious kidney toxicity, Guan Mu Tong has liver toxicity. The dose of nephrotoxicity is lower than the dose of hepatotoxicity. Renal toxicity is the main cause of death of Guan Mu Tong. Aristolochic acid is the main component of causing kidney toxicity. The lethal and nephrotoxic effects of Guan Mu Tong are directly proportional to the dose of aristolochic acid A.