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首页> 外文期刊>Journal of Ethnopharmacology: An Interdisciplinary Journal Devoted to Bioscientific Research on Indigenous Drugs >Hypolipidemic effects and mechanisms of Panax notoginseng on lipid profile in hyperlipidemic rats.
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Hypolipidemic effects and mechanisms of Panax notoginseng on lipid profile in hyperlipidemic rats.

机译：三七对高脂血症大鼠血脂的降血脂作用及其机制。

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Maintenance of normal lipid levels has implicated the involvement of genes induced by liver X receptor alpha (LXRalpha) and Farnesoid X receptor (FXR). This study was designed to evaluate the hypolipidemic effects of n-butanol extract (NE3) of Panax notoginseng (Burk.) F.H. Chen root on lipid homeostasis and investigate the possible mechanisms in animal experiments. In the transactivation assays, NE3 was identified as a dual FXR/LXRalpha agonist. Subsequently, Sprague-Dawley male rats on a high-fat/high-cholesterol diet were treated orally with NE3 or vehicle alone. As expected, the concentrations of serum TC, TG and LDL-C in rats treated with various concentrations of NE3 showed significant (P<0.01) and dose-dependent decrease, respectively, accompanied with a significant (P<0.01) and dose-dependent decrease in the concentration of hepatic TC and TG. Express-level analysis indicated that both LXRalpha target genes including ABCA1, ABCG5, ABCG8 and FXR target genes including ApoCII and SHP were significantly induced by NE3 (P<0.01). Interestingly, LDLR mRNA level was significantly higher by NE3 (P<0.01), accompanied with the significantly decreased expression levels of CYP7A1, ApoCIII and SREBP1c genes (P<0.01). Based on these results, it can be concluded that NE3 as a dual FXR/LXRalpha agonist largely prevented the accumulation of abnormal lipid in the hyperlipidemic rats.
机译：维持正常的脂质水平已经暗示了由肝X受体α（LXRalpha）和法尼醇X受体（FXR）诱导的基因的参与。本研究旨在评估三七（Burax。F.H. Chen）的正丁醇提取物（NE3）对脂质体内稳态的降血脂作用，并研究其在动物实验中的可能机制。在反式激活测定中，NE3被鉴定为双重FXR / LXRalpha激动剂。随后，将高脂/高胆固醇饮食的Sprague-Dawley雄性大鼠口服NE3或单独使用赋形剂治疗。如预期的那样，用不同浓度的NE3处理的大鼠血清TC，TG和LDL-C的浓度分别显示显着（P <0.01）和剂量依赖性降低，同时显着（P <0.01）和剂量依赖性降低肝脏TC和TG的浓度。表达水平分析表明，NE3显着诱导了包括ABCA1，ABCG5，ABCG8在内的LXRalpha靶基因和包括ApoCII和SHP在内的FXR靶基因（P <0.01）。有趣的是，NE3使LDLR mRNA水平显着升高（P <0.01），同时CYP7A1，ApoCIII和SREBP1c基因的表达水平显着降低（P <0.01）。基于这些结果，可以得出结论，NE3作为双重FXR / LXRalpha激动剂，可以在高血脂症大鼠中很大程度上防止异常脂质的蓄积。

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