Ginsenoside Rg1 activates AMPK to inhibit lipid deposition in a cell model of non-alcoholic fatty liver disease

Qing XIAO; Wenxiang HUANG; Shujun ZHANG; Cheng YANG; Jiajun LI; Jinqiu ZHAO; Yue GAO

doi:10.16016/j.1000-5404.201901074

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Ginsenoside Rg1 activates AMPK to inhibit lipid deposition in a cell model of non-alcoholic fatty liver disease

Basic Medicine | 更新时间：2026-01-09

- Ginsenoside Rg1 activates AMPK to inhibit lipid deposition in a cell model of non-alcoholic fatty liver disease
- Journal of Third Military Medical University Vol. 41, Issue 14, Pages: 1343-1349(2019)
- 作者机构：
  
  400016 重庆，重庆医科大学附属第一医院感染科
- 作者简介：
- 基金信息：
  
  the Key Project of Basic Science and Frontier Technology Research of Chongqing Municipal Science and Technology Commission(CSTC2015jcyjBX0079)
- DOI：10.16016/j.1000-5404.201901074
  CLC： R282.71;R285.5;R575.505
- Received：09 January 2019，
  
  Revised：2019-03-11，
  
  Published：30 July 2019
- 稿件说明：
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Qing XIAO, Wenxiang HUANG, Shujun ZHANG, et al. Ginsenoside Rg1 activates AMPK to inhibit lipid deposition in a cell model of non-alcoholic fatty liver disease[J]. Journal of Third Military Medical University, 2019, 41(14): 1343-1349.
DOI：

Qing XIAO, Wenxiang HUANG, Shujun ZHANG, et al. Ginsenoside Rg1 activates AMPK to inhibit lipid deposition in a cell model of non-alcoholic fatty liver disease[J]. Journal of Third Military Medical University, 2019, 41(14): 1343-1349. DOI： 10.16016/j.1000-5404.201901074.

摘要

目的

探讨人参皂苷Rg1对非酒精性脂肪性肝细胞模型脂质沉积的作用及其分子机制。

方法

用0.25 mmol/L棕榈酸处理HepG2细胞24 h构建非酒精性脂肪肝细胞模型；加或不加10 μmol/L AMPK抑制剂(Compound C，CC)预处理1 h，再使用40 μg/mL人参皂苷Rg1或5 μmol/L二甲双胍处理6 h。微量法检测细胞内甘油三酯(triglyceride

TG)含量；油红O染色观察脂滴聚集情况。RT-qPCR及Western blot检测腺苷酸激活蛋白激酶(AMP-activated protein kinase，AMPK)通路相关基因及蛋白的变化。

结果

与对照组比较，模型组细胞内TG、油红O染色吸光度增加(

＜0.05)。Rg1能减少TG及油红O染色吸光度(

＜0.05)。Rg1能增加被棕榈酸抑制的腺苷酸激活蛋白激酶(AMPK)和乙酰辅酶A羧化酶(acetyl-CoA carboxylase，ACC)的磷酸化，下调胆固醇结合调节元件蛋白(sterol regulatory element binding proteins-1c，SREBP-1C)和脂肪酸合成酶(fatty acid synthase，FAS)的表达(

＜0.05)，CC预处理能显著逆转Rg1的改善作用及其对AMPK通路的影响(

＜0.05)。

结论

Rg1可通过调控腺苷酸激活蛋白激酶通路减少非酒精性脂肪性肝病细胞模型脂质沉积。

Abstract

Objective

To investigate the effect of ginsenoside Rg1 on lipid deposition in a cell model of non-alcoholic fatty liver disease (NAFLD) and explore the molecular mechanism.

Methods

HepG2 cells were treated with 0.25 mmol/L palmitic acid for 24 h to induce changes mimicking NAFLD

followed by treatment with 40 μg/mL ginsenoside Rg1 or 5 μmol/L metformin for 6 h with or without pretreatment with 10 μmol/L Compound C (CC

an AMPK inhibitor) for 1 h. The level of triglyceride (TG) in the cells was detected using a micromethod

and the accumulation of lipid droplets was observed using Oil Red O staining. RT-qPCR and Western blotting were employed to detect the alterations in the mRNA and protein expression of the key genes related to the AMPK pathway.

Results

Compared with the control cells

the cell model of NAFLD showed significantly increased intracellular TG level and lipid droplet accumulation (

0.05)

which were both reduced obviously after Rg1 treatment (

0.05). Rg1 significantly abolished palmitic acid-induced inhibition of phosphorylation of intracellular AMPK and acetyl-CoA carboxylase (ACC)

and down-regulated the expression of sterol regulatory element-binding protein-1c and fatty acid synthase (

0.05). Pretreatment with CC significantly antagonized the effects of Rg1 on intracellular TG

lipid deposition and AMPK pathway in palmitic acid-ind

uced cells (

0.05).

Conclusion

Ginsenoside Rg1 can ameliorate lipid deposition in the cell model of NAFLD by activating the AMPK pathway.

关键词

Keywords

references

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