染料木素对油酸诱导HepG2细胞脂质蓄积的影响

张洪敏; 曹世杰; 何昕雅; 邱峰; 张德芹

doi:10.13422/j.cnki.syfjx.20191838

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染料木素对油酸诱导HepG2细胞脂质蓄积的影响

药理 | 更新时间：2021-02-09

- 染料木素对油酸诱导HepG2细胞脂质蓄积的影响
- Effect of Genistein on Oleic Acid-induced Lipid Accumulation in HepG2 Cells
- 中国实验方剂学杂志 2019年25卷第18期页码：71-75
- 作者机构：
  
  天津中医药大学　中药学院，天津市现代中药重点实验室，天津　 301617
- 作者简介：
  
  张洪敏，在读博士，从事中药物质基础研究，E-mail：zhmtlt@163.com
  张德芹，博士，教授，从事中药基本理论及临床应用研究，E-mail：deqin123@163.com
- 基金信息：
  
  国家自然科学基金重点项目(81430095)
- DOI：10.13422/j.cnki.syfjx.20191838
  中图分类号： R2-0; R285.5; R575.5
- 收稿日期：2019-04-12，
  
  网络出版日期：2019-06-04，
  
  纸质出版日期：2019-09-20
- 稿件说明：
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张洪敏, 曹世杰, 何昕雅, 等. 染料木素对油酸诱导HepG2细胞脂质蓄积的影响[J]. 中国实验方剂学杂志, 2019,25(18):71-75.

Hong-min ZHANG, Shi-jie CAO, Xin-ya HE, et al. Effect of Genistein on Oleic Acid-induced Lipid Accumulation in HepG2 Cells[J]. Chinese journal of experimental traditional medical formulae, 2019, 25(18): 71-75.
张洪敏, 曹世杰, 何昕雅, 等. 染料木素对油酸诱导HepG2细胞脂质蓄积的影响[J]. 中国实验方剂学杂志, 2019,25(18):71-75. DOI： 10.13422/j.cnki.syfjx.20191838.

Hong-min ZHANG, Shi-jie CAO, Xin-ya HE, et al. Effect of Genistein on Oleic Acid-induced Lipid Accumulation in HepG2 Cells[J]. Chinese journal of experimental traditional medical formulae, 2019, 25(18): 71-75. DOI： 10.13422/j.cnki.syfjx.20191838.

摘要

目的：

探讨染料木素改善油酸诱导的HepG2细胞脂质蓄积的作用及机制。

方法：

采用不同浓度的油酸处理HepG2细胞24 h诱导建立脂质蓄积模型，12.5，25，50 μmol·L

－1

的染料木素和油酸共同作用于细胞24 h，采用噻唑蓝(MTT)比色法测定细胞存活率，尼罗红和DAPI双染观察细胞内脂滴蓄积情况，并采用试剂盒测定细胞内甘油三酯(TG)含量，蛋白免疫印迹法(Western blot)测定染料木素对脂肪甘油三酯脂肪酶(ATGL)，激素敏感性脂肪酶(HSL)，磷酸化HSL(p-HSL)，沉默信息调节因子1(SIRT1)，过氧化物酶体增殖物激活受体

(PPAR

)，肉毒碱棕榈酰转移酶-1(CPT-1)蛋白表达的影响。

结果：

0.5 mmol·L

－1

油酸及12.5，25，50 μmol·L

－1

染料木素作用细胞24 h对细胞存活率无明显影响；与正常组比较，模型组细胞中TG含量显著升高(

0.01)，细胞内脂滴显著增多(

0.01)，细胞中HSL的磷酸化水平明显下调(

0.05)；与模型组比较，染料木素可明显降低细胞中TG含量(

0.05，

0.01)，明显减少细胞内脂滴(

0.05)，上调细胞中ATGL，p-HSL/HSL，SIRT1，PPAR

，CPT-1蛋白表达水平(

0.05，

0.01)。

结论：

染料木素对HepG2细胞脂质蓄积模型有明显的改善作用，其机制可能通过上调ATGL，p-HSL/HSL，SIRT1，PPAR

，CPT-1蛋白表达水平，进而促进脂质的水解和氧化代谢。

Abstract

Objective:

To explore the effect and mechanism of genistein on oleic acid-induced lipid accumulation in HepG2 cells.

Method:

Lipid accumulation model in HepG2 cells was induced by different concentrations of oleic acid for 24 h

and 12.5

50 μmol·L

-1

genistein and oleic acid acted on cells for 24 h. Cell viability was determined by methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay. Double staining with Nile red and DAPI was used to observe the intracellular lipid droplets. Intracellular triglyceride (TG) content was determined by kit. The protein expression levels of triglyceride lipase(ATGL)

hormone-sensitive fatty acid(HSL)

phosphorylation HSL(p-HSL)

silent information regulator 1(STRT1)

peroxisome proliferator-activated receptor

(PPAR

)

carnitine palmityl transferase 1(CPT-1) in oleic acid-induced HepG2 cells were detected by Western blot.

Result:

0.5 mmol·L

-1

oleic acid and 12.5

50 μmol·L

-1

genistein had no significant effect on cell viability after treated cells for 24 h. Compared with normal group

the TG content and lipid droplets in oleic acid-induced HepG2 cells was significantly increased (

0.01)

and HSL phosphorylation in oleic acid-induced HepG2 cells was significantly down-regulated (

0.05); compared with model group

the TG content and intracellular lipid droplets in HepG2 cells was significantly decreased after administration of genistein (

0.05

0.01). Genistein can significantly up-regulate the protein expression levels of ATGL

p-HSL/HSL

SIRT1

PPAR

and CPT-1 compared with model group (

0.05

0.01).

Conclusion:

Genistein can significantly improve the lipid accumulation in oleic acid-induced HepG2 cells

and its mechanism may be related to up-regulating the protein expression levels of ATGL

p-HSL/HSL

SIRT1

PPAR

CPT-1

and thus promoting lipid hydrolysis and oxidative metabolism.

关键词

Keywords

references

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