降血糖活性成分Bellidifolin遗传毒性研究

Study on the Mutagenesis of Bellidifolin as a Hypoglycemic Component

目的研究降血糖活性成分Bellidifolin的遗传毒性。方法整体试验采用小鼠骨髓嗜多染红细胞微核实验;体外试验采用鼠伤寒沙门菌组氨酸营养缺陷型TA97、TA98、TA100、TA102四个菌株,对Bellidifolin进行Ames实验。结果小鼠骨髓嗜多染红细胞微核发生率结果显示Bellidifolin高、中、低剂量组与阴性对照组比较均差异无显著性(均P>0.05);Ames实验显示,在实验设置浓度和加S9或不加S9的实验条件下,受试物对各菌株所诱发的回变菌落数,均未超过对照的2倍。结论实验结果为阴性,未见Bellidifolin有致突变性作用。

Objective To investigate the genotoxieity of the active hypoglycemic component, Bellidifolin. Methods Bellidifolin was detected by Ames test, the micronucleus test in polychromatic erythocytes from bone marrow in vivo; and in TA97,TA98,TA100 and TA102 strains of salmonella typhimurium with or without the addition of liver microsomal enzyme activation system（＋/-S9） in vitro. Results No obvious difference was found between groups of Bellidifolin and the negative control in the micronucleus test. It was showed that the number of rafutidine induced revertant colonies from different groups didn＇t exceed over two times of those spontaneously formed under the condition with S9 or without S9 in Ames test. Conclusion No mutagenicity was found in Bellidifolin in the test.