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中国精品科技期刊2020
姬妍茹,杨庆丽,张正海,等. 黑菊芋低聚糖对高脂血症小鼠的降血脂作用[J]. 华体会体育,2023,44(4):403−409. doi: 10.13386/j.issn1002-0306.2022050028.
引用本文: 姬妍茹,杨庆丽,张正海,等. 黑菊芋低聚糖对高脂血症小鼠的降血脂作用[J]. 华体会体育,2023,44(4):403−409. doi: 10.13386/j.issn1002-0306.2022050028.
JI Yanru, YANG Qingli, ZHANG Zhenghai, et al. Lipid-lowering Effect of Black Jerusalem Artichoke Oligosaccharide on Hyperlipidemia Mice[J]. Science and Technology of Food Industry, 2023, 44(4): 403−409. (in Chinese with English abstract). doi: 10.13386/j.issn1002-0306.2022050028.
Citation: JI Yanru, YANG Qingli, ZHANG Zhenghai, et al. Lipid-lowering Effect of Black Jerusalem Artichoke Oligosaccharide on Hyperlipidemia Mice[J]. Science and Technology of Food Industry, 2023, 44(4): 403−409. (in Chinese with English abstract). doi: 10.13386/j.issn1002-0306.2022050028.

黑菊芋低聚糖对高脂血症小鼠的降血脂作用

Lipid-lowering Effect of Black Jerusalem Artichoke Oligosaccharide on Hyperlipidemia Mice

  • 摘要: 目的:评价黑菊芋低聚糖对高脂血症小鼠血脂水平的调节功效,初步探究其降血脂的作用机制。方法:依据国标中的辅助降血脂功能评价方法,以高脂饲料饲喂C57BL/6小鼠,建立混合型高脂血症动物模型。将模型动物随机分为模型对照组(MC)、阳性对照组(AC)、黑菊芋低聚糖低、中、高剂量组(OSL,OSM,OSH),同时设空白对照组(CK),每组8只,每只小鼠灌胃量为0.2 mL/d,灌胃时间为46 d。CK组和MC组灌胃生理盐水,AC组给予阿托伐他汀1.0 mg/(kg·bw),黑菊芋低聚糖各组分别灌胃0.25、1.25、2.50 g/(kg·bw)的黑菊芋低聚糖溶液。检测小鼠血脂水平和血清中的超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)以及丙二醛(MDA)含量;观察小鼠肝脏组织形态变化情况,检测肝脏中固醇调节元件结合蛋白-1c(SREBP-1c)和过氧化物酶体增殖物激活受体-γ(PPAR)的表达量。结果:MC组小鼠血清中甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)含量极显著高于CK组(P<0.01),高密度脂蛋白胆固醇(HDL-C)含量极显著低于CK组(P<0.01),说明混合型高脂血症造模成功。黑菊芋低聚糖中、高剂量组小鼠血清中HDL-C水平显著高于MC组(P<0.01或P<0.05),TG和LDL-C水平显著低于MC组(P<0.05),SOD、GSH-Px水平极显著升高(P<0.01),MDA水平极显著降低(P<0.01),SREBP-1c的表达显著下调(P<0.05);小鼠肝脏脂肪样改变有一定程度的减轻。结论:黑菊芋低聚糖对高脂血症小鼠具有改善血脂水平的功效,其降脂作用机制与抗氧化应激及抑制SREBP-1c因子的表达密切相关。

     

    Abstract: Objective: To evaluate the regulating effect of black jerusalem artichoke oligosaccharide on the blood lipid level in hyperlipidemic mice and give a preliminary investigation to the mechanism of lowering blood lipid. Methods: According to the evaluation method of auxiliary hypolipidemic function in the national standard, C57BL/6 mice were fed with high-fat diet to establish a mixed hyperlipidemia animal model. The model animals were randomly divided into MC group (MC), active control group (AC), black jerusalem artichoke oligosaccharide low, medium and high dose groups (OSL, OSM, OSH). At the same time, a blank control group (CK) was set up. There were eight mice in each group, and the dose of gavage was 0.2 mL/d for each mouse. Gavage had lasted for 46 days. CK group and MC group were given normal saline, AC group was given 1.0 mg/(kg·bw) atorvastatin, and black jerusalem artichoke oligosaccharide groups were given 0.25, 1.25, 2.50 g/(kg.bw) black jerusalem artichoke oligosaccharide solution respectively. The blood lipid level and the contents of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) in serum were detected. The morphological changes of mouse liver were observed. The expression of sterol regulatory element binding protein-1c (SREBP-1c) and peroxisome proliferator activated receptor-γ (PPAR-γ) in mouse liver were detected. Results: The triglyceride (TG), total cholesterol (TC) and low density lipoprotein cholesterol (LDL-C) in the MC group were significantly higher than those in the CK (P<0.01), and the high density lipoprotein cholesterol (HDL-C) were significantly lower than those in the CK (P<0.01), indicating that the mixed hyperlipidemia was successfully modeled. The levels of HDL-C in the medium and high dose groups of black jerusalem artichoke oligosaccharide were significantly higher than those in the MC group (P<0.01 or P<0.05), the levels of TG and LDL-C were significantly lower than those in the MC group (P<0.05), the levels of SOD and GSH-Px were significantly increased (P<0.01), the level of MDA was significantly reduced (P<0.01), and the expression of SREBP-1c was significantly decreased (P<0.01). The fatty changes of mouse liver were alleviated to a certain degree. Conclusion: The black jerusalem artichoke oligosaccharide could improve the blood lipid level of hyperlipidemic mice, and the lipid-lowering mechanism was closely related to the antioxidant stress and the inhibition of SREBP-1c expression.

     

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