氯原酸对高脂膳食喂养的ApoE-/-小鼠动脉粥样硬化改善效应的研究  

EFFECT OF CHLOROGENIC ACID ON PROGRESS OF ATHEROSCLEROSIS IN APOE-/-MICE FED HIGH FAT DIET

作　　者：靳沙沙 李淑媛[2] 陈志民[1] 谢岚[1] 常翠青[1] 

机构地区：[1]北京大学第三医院运动医学研究所,北京100191 [2]山东大学附属省立医院手足外科,济南250021

出　　处：《营养学报》2013年第5期440-444,共5页Acta Nutrimenta Sinica

基　　金：国家自然科学基金(No.30872112)

摘　　要：目的探讨氯原酸(chlorogenic acid,CGA)对高脂膳食喂养的ApoE-/-小鼠动脉粥样硬化进程的影响。方法22只7w龄雄性ApoE-/-小鼠随机分为对照组和氯原酸两组,均给予21%高脂膳食,CGA组采用灌胃方式给予CGA80 mg/(kg bw·d)。12w后,观察胸主动脉病理变化,检测血脂和肝脏抗氧化酶活性,以及过氧化物酶体增生物激活受体(PPARs)表达情况。结果与对照组相比,CGA组血清中甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白(LDL-C)分别显著下降34%(P<0.01)、16%(P<0.05)和24%(P<0.01);动脉粥样硬化指数(ASI)显著下降16%(P<0.05);血清和内脏脂肪中肿瘤坏死因子-α(TNF-α)水平分别显著降低63%(P<0.05)和21%(P<0.01);肝脏脂质过氧化物(LPO)含量降低41%(P<0.05),超氧化物歧化酶(SOD)的活性显著增高(P<0.05);肝脏PPAR-β的mRNA和蛋白表达水平均显著上调(P<0.05)。结论 CGA增强了肝脏抗氧化能力,抑制脂质过氧化,并且上调肝脏PPAR-β表达,改善血脂紊乱和炎症反应,最终延缓高脂膳食喂养的ApoE-/-小鼠动脉粥样硬化的进程。Objective To investigate the effect of chlorogenic acid （CGA） on the progress of atherosclerosis （AS） in high fat diet fed ApoE-/- mice. Methods Twenty-two 7 w old ApoE-/ mice were randomly divided into the control group and CGA group. Both groups were fed high fat diet, while CGA group was given CGA 80mg/kg bw per day through intragastric administration for 12 w. The pathological changes of the thoracic aorta were observed by microscope. Serum lipids and antioxidant enzyme activities in liver were detected, as well as the expression of peroxisome proliferator-activated receptors （PPARs） in liver. Results Compared with control group, the levels of TG, TC and LDL-C in CGA group were significantly reduced by 34% （P〈0.01 ）, 16% （P〈0.05） and 24% （P〈0.01 ） respectively. The atberosclerosis index （ASI） was significantly decreased by 16 % （P〈0.05） . The level of TNF-c~ in serum and visceral fat was significantly decreased by 63% （P〈0.05） and 21% （P 〈0.01 ） respectively. The LPO content in liver was reduced by 41% （P〈0.05） and the activity of SOD was elevated by 25% （P 〈0.05） . The expression of mRNA and protein level of PPAR-[3 was both significantly increased （P 〈0.05）. Conclusion CGA could inhibit the progress of AS in high fat diet fed ApoE-/- mice, possibly via increasing the antioxidative ability of liver to inhibit the lipid peroxidation, as well as regulating the expression of PPAR-[3 to improve dyslipidemia and inflammatory responses.

关 键 词：氯原酸 动脉粥样硬化 脂质过氧化 炎性因子 PPARS 

分 类 号：R543.5[医药卫生—心血管疾病]