| 刘才冬 侯亚义 蒋云 金铃.银灵通胶囊调节实验性高脂饮食大鼠血脂的研究[J].,2015,15(26):5038-5041 |
| 银灵通胶囊调节实验性高脂饮食大鼠血脂的研究 |
| The Study of Regulating SerumLipids by Yinlingtong Capsules inExperimental High-fat Diet |
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| DOI： |
| 中文关键词: 银灵通胶囊 脂质代谢 动脉粥样硬化 |
| 英文关键词: Yinlingtong capsules Lipid metabolism Atherosclerosis |
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| 中文摘要: |
| 目的：探究银灵通胶囊对脂质代谢的影响及其机制。方法：建立大鼠高脂模型，用药后检测其血脂、丙二醛（MDA）、超氧化物
歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH-Px）的活性，检测肝脏组织的高密度脂蛋白受体SR-BI、低密度脂蛋白受体（LDLR）、
氧化低密度脂蛋白( ox- LDH )受体CD36 蛋白表达的mRNA表达水平,检测血管组织学变化。结果：高脂饮食明显升高大鼠血清
中总胆固醇（CH）、甘油三酯（TG）、低密度脂蛋白胆固醇（LDL-C）和动脉硬化指数（AI值），银灵通胶囊组可降低上述指标，且呈一
定的浓度依赖；高脂饮食可增加肝脏中SR-BI 及CD36 表达，降低LDLR 表达，银灵通胶囊引起SR-BI的过度表达，使LDLR 表
达增加，CD36 表达下降。高脂饮食使血清中MDA的含量增加，给予银灵通胶囊后，明显降低血清MDA 的含量。结论：银灵通胶
囊具有调节脂质代谢，抗动脉粥样硬化（AS）及抗脂质过氧化作用。其机制与银灵通胶囊能引起肝脏中SR-BI 的过度表达及
LDLR 表达增加，降低肝脏中CD36 表达和血清MDA含量有关。 |
| 英文摘要: |
| Objective:To explore the mechanism of Yinlingtong capsules to lipid metabolism.Methods:After rat hyperlipidemia
model was prepared by the high-fat diet, the different doses Yinlingtong capsules were administered by one time every two days. Atfer
three consecutive months, the serum lipid, malonic aldehyde (MDA), superoxide dismutase (SOD)and the activity of glutathione peroxidase
(GSH-Px), high density lipoprotein receptor SR-BI, LDL receptor (LDLR), oxidation of low-density lipoprotein (ox-LDH detection
of liver tissue) receptors CD36 protein expression of mRNA levels and the vascular histological changes were detected.Results:The
serum total cholesterol (CH), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C) and atherogenic index (AI values) of the
high-fat diet were significantly increased in the high-fat rat, and Yinlingtong capsules could reduce the above-mentioned indicators a dose
dependent. Fat diet can increase the liver in SR-BI and CD36 expression, reduce LDLR expression, and Yinlingtong capsules leaded to
the overexpression of SR-BI LDLR and decrease of CD36 expression. High-fat diet increased serum MDA content, and Yinlingtong capsules
could significantly lower serumMDA content.Conclusion:Yinlingtong capsules could regulate lipid metabolism, anti-atherosclerosis
(AS), and anti-lipid peroxidation in the high-fat rat. The mechanisms were related with overexpression of SR-BI, LDLR in the liver
and reducing CD36 expression in the liver and serumMDA. |
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