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中国临床药理学与治疗学 ›› 2017, Vol. 22 ›› Issue (8): 870-874.

• 基础研究 • 上一篇    下一篇

深海鱼油对高脂血症模型大鼠血脂的影响及机制探讨

谢 珍,康 桦,何立成,匡 荣   

  1. 浙江省食品药品检验研究院,杭州 310052,浙江
  • 收稿日期:2017-01-09 修回日期:2017-02-14 出版日期:2017-08-26 发布日期:2017-08-18
  • 通讯作者: 匡荣,男,博士,主任药师,硕士生导师,研究方向:药理/毒理学。 Tel:0571-86457970 E-mail:kuangrong@zjyj.org.cn
  • 作者简介:谢珍,女,硕士,药师,研究方向:药理/毒理学。 E-mail:cheerxie@163.com
  • 基金资助:

    浙江省药品接触材料质量控制研究重点实验室(2014E10006)

Effects and mechanism of deep-sea fish oil on blood lipid in hyperlipidemia rats

XIE Zhen, KANG Hua, HE Licheng, KUANG Rong   

  1. Zhejiang Institute of Food and Drug Control, Hangzhou 310052, Zhejiang, China
  • Received:2017-01-09 Revised:2017-02-14 Online:2017-08-26 Published:2017-08-18

摘要:

目的: 探讨深海鱼油对高脂血症模型大鼠血脂的影响及相关机制。方法: 高脂饲料喂养大鼠建立混合型高脂血症动物模型,设空白对照组,模型对照组,深海鱼油三个剂量组(250、500、1 500 mg/kg),每组12只,空白对照组、模型对照组均同时给予同体积的大豆油,连续灌胃40 d后,检测血清中总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)及高密度脂蛋白胆固醇(HDL-C)含量并计算动脉粥样硬化指数(AI1、AI2)及冠心指数(R-CHR);检测血清和肝组织中超氧化物歧化酶(SOD)、丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-Px)的活性,利用Western blot测定肝组织中沉默信息调节因子1(SIRT1)、过氧化物酶体增殖物激活受体-α(PPAR-α)蛋白表达的变化。结果: 与模型对照组相比,深海鱼油各剂量组均可明显降低大鼠血清TC、TG、LDL-C的含量,中、高剂量均可使AI1、AI2及R-CHR显著下降。高脂血症大鼠血清和肝组织氧化应激水平增高,在血清中,中、高剂量组大鼠SOD、GSH-Px活性均显著增加,MDA水平显著下降;在肝组织中,中、高剂量组SOD、GSH-Px活性均显著增加,低、中、高剂量组MDA水平显著下降;中、高剂量的深海鱼油可增加肝脏SIRT1、PPAR-α的蛋白表达量。结论:深海鱼油可降低高脂血症大鼠血脂水平,其作用机制可能与其在一定程度上增强血清和肝组织抗氧化酶类活性,清除脂质过氧化物及提高SIRT1、PPAR-α的蛋白表达量有关。

关键词: 深海鱼油, 血脂, 抗氧化, 沉默信息调节因子1, 过氧化物酶体增殖物激活受体-α

Abstract:

AIM: To investigate the regulation effect of deep-sea fish oil for blood lipid of rat models with hyperlipidemia and its possible mechanism. METHODS: Rats models with mixed hyperlipidemia were established by feeding high-fat diet and were divided into control group, model group and three deep-sea fish oil treatment groups (250, 500, 1 500 mg/kg), with 12 rats in each. The control group and model group received equal volume of soybean oil, while the treatment groups were administered with deep-sea fish oil for 40 days. Changes in TC,TG,HDL-C,LDL-C of serum were compared, and atherosclerosis index(AI1, AI2),R-CHR indexes were calculated. Activities of SOD,MDA,GSH-Px in serum and liver tissue were measured by kits. Protein expression levels of SIRT1,PPAR-α were detected by Western blot. RESULTS: Compared with model group, levels of TC,TG,LDL-C in treatment groups were significantly decreased, and AI1,AI2 and R-CHR indexes in middle and high dose groups were significantly decreased. Oxidative stress was increased in hyperlipidemia rats of its serum and liver. In serum, the SOD,GSH-Px levels in high and middle dose groups were significantly increased, while the level of MDA decreased remarkably. In liver, the SOD,GSH-Px levels in middle and high dose groups were significantly increased, the level of MDA in three treatment groups decreased remarkably. Middle and high dose of deep-sea fish oil increased the protein expressions of SIRT1 and PPAR-α in liver. CONCLUSION: Deep-sea fish oil can moderate blood lipid in hyperlipidemia rats, which is probably associated with the regulation of the response level to oxidative stress in serum and liver and improving expression level of the SIRT1 and PPAR-α proteins.

Key words: deep-sea fish oil, blood lipid, antioxidation, SIRT1, PPAR-α

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