青葙总皂苷对高血脂动物脂质代谢的影响

Pharmacodynamic study of total celosins on anti-hyperlipidemia

目的探讨青葙总皂苷(CES)对高血脂动物脂质代谢的影响。方法建立金黄地鼠、家兔高血脂模型,对实验动物血液和肝组织脂质指标和脂质过氧化指标进行检测,并对动物肝脏进行病理组织学观察。结果经口给予CES 10～90mg/kg两周,可降低高血脂金黄地鼠血清和肝脏组织中血清总胆固醇(TC),甘油三酯(TG)和低密度脂蛋白胆固醇(LDLc)含量(P<0.05或P<0.01);经口给予高血脂家兔CES 6～24.0mg/kg,给药10d时,可降低血清TC和LDL-c含量(P<0.01);给药20d和30d,不仅降低了血清TC、LDL-c含量(P<0.01),还降低了TG含量(P<0.05),表现出作用持续时间长而平稳的特点。同时,CES还可降低肝脏组织中TC、TG含量(P<0.05)和丙二醛(MDA)、血清脂肪酶(LPS)含量(P<0.05)。病理组织学观察显示:家兔模型组肝细胞胞浆内脂肪堆积明显,肝细胞受损程度严重,有大面积点状坏死现象。随着CES给药剂量的增加,肝细胞胞浆内脂肪堆积明显减少,肝细胞受损程度也明显减轻。结论 CES对动物高血脂脂代谢紊乱有明显治疗作用,其对高血脂脂代谢紊乱的治疗作用可能与其降低肝组织中MDA和LPS的含量有关。

Objective To study the effect of total saponin（CES）on lipid metabolism in hyperlipidemic animals.Methods Golden hamster and rabbit hyperlipidemia animal models were established for this study.Both hyperlipidemia models were achieved by feeding high fat diet.The blood,hepatic lipid parameters and lipid peroxidation index were detected.Liver pathological changes were recorded.Results CES were orally administered to golden hamster hyperlipidemia model for two weeks at doses of 10-90 mg/kg.TC,TG and LDL-c were significantly reduced both in the serum and liver.In rabbit hyperlipidemia model,CES was orally administered at 6.0-24.0 mg/kg.Serum TC and LDL-c were reduced at day 10.Significant reduction of serum TC,LDL-c levels（P〈0.01）and TG content（P〈0.05）were observed after 20 and 30 days.This lipid-lowing effect was long lasting and stable.At the meantime,CES can also decrease the liver tissue TC,TG content（P〈0.05）and MDA,LPS content（P〈0.05）.Pathological section showed that fat was significantly accumulated in the liver cell cytoplasm in rabbit model group.The liver cells were damaged.Large area of spotty necrosis was observed.Fat accumulation in the cytoplasm was significantly decreased in CES groups with dose dependent manner.With increased CES dose,liver damage was ameliorated.Conclusion CES can effectively reduce lipids in different animal hyperlipidemia models.This effect may be related to the decrease of the content of MDA and LPS in liver.