黄芪多糖对高脂血症大鼠血脂的调节

Effect of astragalus polysaccharide in regulating blood lipid of rats with hyperlipidemia

目的:观察黄芪多糖对高脂饲料诱导的高脂血症大鼠血脂水平,肝脏脂质沉积以及机体抗氧化能力的影响,与疗效确切的降脂药非诺贝特作用结果进行比较。方法:实验于2004-9/2004-12空军总医院实验动物中心完成。①选用健康雄性Wistar大鼠60只。按体质量随机分为6组,每组10只:正常对照组(饲喂普通饲料),高脂模型组[饲喂高脂饲料(主要成分:普通饲料0.788、猪油0.1、蛋黄粉0.1、胆固醇0.01和胆酸盐0.002),黄芪多糖高、中、低剂量组[分别将黄芪多糖(颗粒剂型,国食健字G20040383,生产批号20040301,由解放军总医院科技开发中心提供)以16.68,8.34,3.52g/kg的剂量加入高脂饲料进行喂养],非诺贝特组[将非诺贝特胶囊(由法国利博福尼制药公司制造,200mg/粒,批号78879)以0.067g/kg的剂量加入高脂饲料进行喂养]。6组动物均连续喂养12周,每周测体质量。②喂养12周后,取肝组织称质量,计算肝指数(肝指数=肝质量/体质量×100%)。用酶法测定血清和肝组织总胆固醇、三酰甘油水平和含量;用免疫比浊法测定血清高密度脂蛋白胆固醇、低密度脂蛋白胆固醇水平;用硫代巴比妥酸反应测定血清和肝组织丙二醛水平和含量;用微弱化学发光方法测定血清和肝组织超氧化物歧化酶活力;用速率法测定血清和肝组织谷胱甘肽过氧化物酶活力。③计量资料差异比较采用方差分析,两两比较采用LSD检验。结果:大鼠60只均进入结果分析。①非诺贝特组,黄芪多糖高、中、低剂量组大鼠血清总胆固醇,低密度脂蛋白胆固醇和非诺贝特组三酰甘油均明显低于模型组(P<0.05)。而高密度脂蛋白胆固醇均明显低于正常对照组(P<0.05),但与模型组比较,差异不明显(P>0.05)。非诺贝特组,黄芪多糖高、中、低剂量组体质量增长值低于高脂模型组,但差异不明显(P>0.05)。②黄芪多糖高、中、低剂量组大鼠肝脏总胆固醇和黄芪多糖高剂量组的三酰甘油含量明显低于模型组(P<0.01);黄芪多糖中、低剂量组大鼠肝脏三酰甘油含量低于模型组,但差异不明显(P>0.05)。黄芪多糖高、中剂量组肝指数明显高于正常对照组(P<0.01,0.05),但明显低于模型组(P<0.05)。非诺贝特组的肝脏总胆固醇明显低于模型组(P<0.05),但三酰甘油含量和肝指数与模型组相近(P>0.05)。③黄芪多糖高、中剂量组大鼠肝组织丙二醛含量明显低于模型组(P<0.01,0.05),超氧化物歧化酶活力明显高于模型组(P<0.05)。黄芪多糖低剂量组大鼠肝组织丙二醛含量和超氧化物歧化酶活力与模型组相近。黄芪多糖各剂量组肝组织谷胱甘肽过氧化物酶活力与模型组差异不明显(P>0.05)。非诺贝特组大鼠肝脏丙二醛含量,超氧化物歧化酶活力无显著变化(P>0.05),但谷胱甘肽过氧化物酶活力明显低于模型组(P<0.05)。④黄芪多糖高、中剂量组大鼠血清丙二醛水平明显低于模型组(P<0.01),谷胱甘肽过氧化物酶活力明显高于模型组(P<0.01);黄芪多糖低剂量组大鼠血清谷胱甘肽过氧化物酶活力明显高于模型组(P<0.05),丙二醛低于模型组,但差异不明显(P>0.05);而各组超氧化物歧化酶均与模型组相近(P>0.05)。非诺贝特组大鼠血清丙二醛水平明显低于模型组,谷胱甘肽过氧化物酶活力明显高于模型组(P<0.01)。结论:黄芪多糖可降低高脂血症大鼠的血脂,减少肝脏脂质沉积,提高肝脏和血液的抗氧化能力,减轻高脂饮食导致的氧化损伤。非诺贝特虽可降低血脂,但因促进脂质的肝脏代谢,而加重肝脏的损伤。

AIM： To study the effect of astragalus polysaccharide on level of blood lipid, lipid deposition in liver and the antioxidant ability in rat with hyperlipidemia induced by high lipid diet so as to compare with the effect of fenofibrate. METHODS： The experiment was completed in the Laboratory Animal Center of the General Hospital of Air Force of Chinese PLA between September and December 2004. ① Sixty healthy male Wistar rats were randomly divided into 6 groups according to body mass： normal control group （fed with common feed）, high lipid model group （main component： 0.788 common feed, 0.1 lard, 0.1 yolk powder, 0.01 cholesterol and 0.002 cholic acid salt）, high, middle and low dose groups of astragalus polysaccharide （16.68 g/kg, 8.34 g/kg and 3.52 g/kg astragalus polysaccharide were added in high lipid feed respectively; drug granules; national healthy number： G20040383; batch number： 20040301; provided by Technological Developing Center of General Hospital of Chinese PLA）, and fenofibrate group （0.067 g/kg fenofibrate was added in high lipid feed; provided by Laboratoires FOURNIER SA; 200 mg/pill; batch number： 78879） with 10 in each group. Rats in the 6 groups were fed for 12 weeks and their body mass was measured each week. ② After 12 weeks, hepatic tissue was weighted to calculate hepatic index （hepatic index = hepatic mass/body mass × 100%）. Levels and contents of total cholesterol （TC） and tfiglyceride （TG） in serum and hepatic tissue were assayed with enzyme method; levels of high density lipoprotein cholesterol （HDLC） and low density lipoprotein cholesterol （LDLC） were assayed with immune turbidimetry; levels and contents of malondialdehyde （MDA） in serum and hepatic tissue were assayed with thiobarbituric acid reaction; activity of superoxide dismutase （SOD） was assayed with mild chemiluminescence; activity of glutathione peroxidase was assayed with velocity method. ③ Measurement data were compared with analysis of variance, and differences between groups were compared with LSD test. RESULTS： All the 60 mice were involved in the analysis of results. ① Contents of TC and LDLC in fenofibrate group, high, middle and low dose groups of astragalus polysaccharide and content of TG in fenofibrate group were all lower than those in model group （P 〈 0.05）, and content of HDLC was lower than that in normal control group （P 〈 0.05）, but there was not significant difference as compared with that in model group （P 〉 0.05）. Increases of body mass in fenofibrate group, high, middle and low dose groups of astragalus polysaccharide were lower than that in high lipid model group, but there was not significant difference （P 〉 0.05）.②Contents of TC in high, middle and low dose groups of astragalus polysaccharide and content of TG in high dose group of astragalus polysaccharide were lower than those in model group （P 〈 0.01）, and contents of TG in middle and low dose groups of astragalus polysaccharide were lower than those in model group, but there was not significant difference （P 〉 0.05）. Hepatic index in high and middle dose groups of astragalus polysaccharide was higher than that in normal control group （P 〈 0.01, 0.05）, but was lower than that in model group （P 〈 0.05）. Content of TC in fenofibrate group was lower than that in model group （P〈 0.05）, but content of TG and hepatic index were similar to those in model group （P 〉 0.05）. ③Contents of MDA in high and middle dose groups of astragalus polysaccharide were lower than those in model group （P 〈 0.01, 0.05）, and activity of SOD was higher than those in model group （P 〈 0.05）. Content of MDA and activity of SOD in low dose group of astragalus polysaccharide were similar to those in model group. Activity of glutathione peroxidase was not significant difference between dosage groups and model group （P 〉 0.05）. Content of MDA and activity of SOD in fenofibrate group was not changed remarkably （P 〉 0.05）, but activity of glutathione peroxidase was lower than that in model group （P 〈 0.05）.④Contents of MDA in high and middle dose groups of astragalus polysaccharide were lower than those in model group （P 〈 0.01）; activity of glutathione peroxidase was higher than that in model group （P 〈 0.01）; activity of glutathione peroxidase in low dose groups of astragalus polysaccharide was higher than that in model group （P 〈 0.05）; content of MDA was lower than that in model group, but there was not significant difference （P 〉 0.05）. Activity of SOD in each group was similar to that in model group （P〉 0.05）. Level of MDA in fenofibrate group was lower than that in model group, but activity of glutaihione peroxidase was higher than that in model group （P 〈 0.01）. CONCLUSION： Astragalus polysaccharide can decrease level of blood lipid, reduce lipid deposition in liver, raise the antioxidant ability of serum and liver tissue, and relieve oxidation injury of rat with hyperlipidemia induced by high lipid diet. Fenofibrate can decrease level of blood lipid and deteriorate hepatic injury because of improving hepatic metabolism of lipid.