甘草总黄酮对高脂血症模型小鼠的干预作用

目的：ApoE^-／-小鼠，给予甘草总黄酮（GTF）干预，探索其调脂、抗氧化作用，进而研究其防治动脉粥样gZ-fG（AS）形成的作用。方法：健康雄性ApoE基因敲除小鼠30只，9周龄，适应性饲养1周，随机分成5组：模型组；阳性对照（银杏叶片）组；GTF高、中、低剂量组，每组6只，分别给药。另取8周龄正常C57BL／6j小鼠6只为正常对照组（给予普通饲料喂养）；正常对照组、模型组给以等容剂量生理盐水，连续干预4周。末次给药后次日处死小鼠，摘眼球取血，分离血清，检测相应指标；分离肝脏，制作切片，观察肝脏病理改变。结果：模型组血脂、脂质过氧化产物（MDA）、超氧化物歧化酶活力（SOD）、氧化性低密度脂蛋白（ox—LDL）水平及肝脏形态学显示造模成功。GTF高、中剂量可有效降低血清TC、TG、LDL—C。升高HDL—C水平，抑制MDA及ox—LDL形成，增强SOD活性，提高机体抗氧化能力，对AS发生发展有抑制作用。结论：14周龄ApoE^-／-小鼠血脂水平异常，伴随氧化反应增强、抗氧化活力降低等反应，GTF通过调节血清脂质、脂蛋白胆固醇水平，亦可抑制氧化损伤减少ox—LDL的产生进而防止或延缓AS的形成。

Interention Effect of Total Flavonoids of Gycyrrhiza on Hyperlipidenia Model Mice

Objective：ApoE-/- mice were given licorice flavonoids （GTF） intervention, explore its lipid, antioxidant effect, and thus to study the prevention and treatment of AS formation mechanism. Methods： 30 healthy male ApoE knockout mice, 9 weeks old, adaptive feeding one week, were randomly divided into five groups： model group; positive control （Ginkgo biloba） group; GTF high, medium and low dose groups, administered separately. Another 8-week-old normal C57BL/6J mice as normM control group （given normal diet）; nor- mal control group, model group given isovolumetrie normal saline, continuous intervention for 4 weeks. The day after the last administra- tion, the mice were killed, eyeball blood serum was separated, detected corresponding indicators; separation of the liver, making slices, observe pathological changes in the liver. Results： The model group lipids, lipid peroxidation （MDA）, superoxide dismutase activity （SOD）, oxidized low-density lipoprotein （ox-LDL） levels and liver morphology shows successful model. GTF high dose can effectively re- duce serum TC, TG, LDL, raise HDL levels, inhibit the formation of MDA and ox-LDL, enhanced SOD activity and increased antioxidant capacity, on the development of AS inhibition. Conclusion： 14-week-old ApoE-/- mice abnormal lipid levels, accompanied by oxida- tion enhanced antioxidant activity and decreased reaction, GTF by regulating serum lipids, lipoproteins, also inhibit oxidative damage to reduce the generation of ox-LDL and thus prevent or delay the formation of AS.