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通过激活 SREBP-2 和 LDL 受体,刺五加具有降低胆固醇的作用。

Cholesterol-lowering effect of Aralia elata (Miq.) Seem via the activation of SREBP-2 and the LDL receptor.

机构信息

Department of Agrofood Resources, National Academy of Agricultural Science, RDA, Wanju-Gun, Jeollabuk-do, Republic of Korea.

Department of Agrofood Resources, National Academy of Agricultural Science, RDA, Wanju-Gun, Jeollabuk-do, Republic of Korea.

出版信息

J Chin Med Assoc. 2017 Oct;80(10):630-635. doi: 10.1016/j.jcma.2017.06.007. Epub 2017 Jul 6.

Abstract

BACKGROUND

Hyperlipidemia causes arteriosclerosis, a risk factor for coronary heart disease. Prevention of hyperlipidemia by improving dietary habits has recently attracted attention. In this regard, we investigated whether Aralia elata (Miq.) Seem (AE) extract inhibits hepatic cholesterol accumulation and modulate the cellular signaling pathway.

METHODS

To determine AE's cholesterol regulating mechanism, we measured cholesterol level, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase activity and cholesterol regulating-related gene expression in HepG2 cells and in high-fat diet (HFD)-induced mice using ELISA and RT-PCR assay.

RESULTS

The AE extract reduced cholesterol levels and HMG-CoA reductase activity in hepatocellular carcinoma HepG2 cells. In addition, it also reduced the plasma cholesterol concentrations in HFD-induced mice. Furthermore, the AE extract increased the gene expression of the LDL-receptor (LDL-R); sterol-regulatory-element binding protein-2 (SREBP-2); ATP-binding cassette, sub-family A, member 1 (ABCA1); and scavenger receptor class B member 1 (SR-B1) in a dose-dependent manner. However, the AE extract did not affect the gene expression of acetyl-coenzyme A acetyltransferase (ACAT) in either the HepG2 cells or mice.

CONCLUSION

We demonstrated that the AE extract activated genes related to cholesterol metabolism, such as SREBP-2 and LDL-R, which resulted in hypocholesterolemic activities.

摘要

背景

高血脂会导致动脉粥样硬化,是冠心病的一个风险因素。通过改善饮食习惯来预防高血脂症最近引起了人们的关注。在这方面,我们研究了花旗参(Miq.)提取物是否能抑制肝脏胆固醇积累并调节细胞信号通路。

方法

为了确定 AE 的胆固醇调节机制,我们使用 ELISA 和 RT-PCR 测定了 HepG2 细胞和高脂饮食(HFD)诱导的小鼠中的胆固醇水平、3-羟-3-甲基戊二酰辅酶 A(HMG-CoA)还原酶活性和胆固醇调节相关基因的表达。

结果

AE 提取物降低了肝癌 HepG2 细胞中的胆固醇水平和 HMG-CoA 还原酶活性。此外,它还降低了 HFD 诱导的小鼠血浆胆固醇浓度。此外,AE 提取物以剂量依赖性方式增加了低密度脂蛋白受体(LDL-R)、固醇调节元件结合蛋白-2(SREBP-2)、ATP 结合盒,亚家族 A,成员 1(ABCA1)和清道夫受体 B 类成员 1(SR-B1)的基因表达。然而,AE 提取物对 HepG2 细胞或小鼠中的乙酰辅酶 A 乙酰转移酶(ACAT)基因表达没有影响。

结论

我们证明了 AE 提取物激活了与胆固醇代谢相关的基因,如 SREBP-2 和 LDL-R,从而发挥了降胆固醇作用。

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