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目的 研究抗肝炎药联苯双酯对大鼠黄曲霉毒素B1代谢和肝毒性的影响。方法 大鼠po联苯双酯 30 0mg·kg-1·d-1,连服 3d后ip黄曲霉毒素B11 5mg·kg-1。给黄曲霉毒素B116h后测定血清ALT和AST水平 ,观察联苯双酯对黄曲霉毒素B1引起肝损伤的保护作用以及对体外代谢的影响。结果 联苯双酯(30 0mg·kg-1·d-1,连服 3d)可明显降低黄曲霉毒素B1引起的大鼠血清转氨酶升高 ,增加低毒代谢产物AFM1的生成。联苯双酯还可增加大鼠肝脏细胞色素P4 5 0总量和胞浆GSH含量 ,诱导P4 5 0 2B1介导的PROD和GST的活性。此外 ,联苯双酯对P4 5 0 3A介导的红霉素脱甲基酶和P4 5 0 1A介导的EROD也有一定的诱导作用。结论 联苯双酯可通过增加大鼠肝脏对AFB1代谢的解毒功能起到肝保护作用。
Objective To study the effect of anti-hepatitis B-diphenylester on aflatoxin B1 metabolism and hepatotoxicity in rats. Methods The rats were given dipyridamole 30 0 mg · kg-1 · d-1 and aflatoxin B11 5 mg · kg-1 for 3 days. Aflatoxins B116h serum ALT and AST levels were observed after bifendate aflatoxin B1-induced liver injury and its impact on metabolism in vitro. Results Bifendate (300 mg · kg-1 · d-1 for 3 days) could significantly reduce the increase of serum aminotransferase induced by aflatoxin B1 and increase the production of low toxic metabolite AFM1. Bifendate also increased the total amount of cytochrome P450 and cytosolic GSH in the liver and induced the P450B2-mediated activity of PROD and GST. In addition, bifendate also induced P450 3A-mediated erythromycin demethylase and P450 1A-mediated EROD. Conclusion Bifendate can play a protective role in liver by increasing the detoxification of AFB1 metabolism in rat liver.