Ginsenosides from stems and leaves of ginseng prevent ethanol-induced lipid accumulation in human L02 hepatocytes

Chao-feng Hu; Li-ping Sun; Qin-he Yang; Da-xiang Lu; Sen Luo

doi:10.1007/s11655-016-2617-8

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Ginsenosides from stems and leaves of ginseng prevent ethanol-induced lipid accumulation in human L02 hepatocytes

Updated：2021-08-27

- Ginsenosides from stems and leaves of ginseng prevent ethanol-induced lipid accumulation in human L02 hepatocytes
- Chinese Journal of Integrative Medicine Vol. 23, Issue 6, Pages: 438-444(2017)
- Affiliations：
  
  1. Department of Pathophysiology, Key Laboratory of State Administration of Traditional Chinese Medicine of the People’s Republic of China, Medical College, Jinan University,Guangzhou,China
  2. Department of Nephrology, Shenzhen People’s Hospital, Second Clinical Medical College of Jinan University,Guangdong Province,Shenzhen,China
  3. Department of Traditional Chinese Medicine, Medical College, Jinan University,Guangzhou,China
- Author bio：
- Funds：
  
  Supported by Natural Science Foundation of Guangdong Province, China (No. S2012010008161)
- DOI：10.1007/s11655-016-2617-8
  CLC：
- Published：2017，
  
  Published Online：10 September 2016，
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Hu, Cf., Sun, Lp., Yang, Qh. et al. Ginsenosides from stems and leaves of ginseng prevent ethanol-induced lipid accumulation in human L02 hepatocytes., Chin. J. Integr. Med. 23, 438–444 (2017). https://doi.org/10.1007/s11655-016-2617-8

Chao-feng Hu, Li-ping Sun, Qin-he Yang, et al. Ginsenosides from stems and leaves of ginseng prevent ethanol-induced lipid accumulation in human L02 hepatocytes. [J]. Chinese Journal of Integrative Medicine 23(6):438-444(2017)
Hu, Cf., Sun, Lp., Yang, Qh. et al. Ginsenosides from stems and leaves of ginseng prevent ethanol-induced lipid accumulation in human L02 hepatocytes., Chin. J. Integr. Med. 23, 438–444 (2017). https://doi.org/10.1007/s11655-016-2617-8 DOI：

Chao-feng Hu, Li-ping Sun, Qin-he Yang, et al. Ginsenosides from stems and leaves of ginseng prevent ethanol-induced lipid accumulation in human L02 hepatocytes. [J]. Chinese Journal of Integrative Medicine 23(6):438-444(2017) DOI： 10.1007/s11655-016-2617-8.

摘要

To investigate the effect of ginsenosides from stems and leaves of ginseng on ethanol-induced lipid deposition in human L02 hepatocytes. L02 cells were exposed to ethanol for 36 h and treated with or without ginsenosides. The viability of L02 cells was evaluated by methylthiazolyldiphenyl-tetrazolium bromide assay and the triglyceride (TG) content was detected. Lipid droplets were determined by oil red O staining. Intracellular reactive oxygen species (ROS) production and the mitochondrial membrane potential were tested by flow cytometry. The ATP level was measured by reverse phase high performance liquid chromatography. The expression of cytochrome p450 2E1 (CYP2E1) and peroxisome proliferator-activated receptor α (PPARα) was detected by reverse transcriptase-polymerase chain reaction and Western blotting

respectively. Ethanol exposure resulted in the increase of TG level

lipid accumulation and ROS generation

and the decrease of mitochondrial membrane potential and ATP production in the cells. However

ginsenosides significantly reduced TG content (9.69±0.22 μg/mg protein vs. 4.93±0.49 μg/mg protein

P<0.01)

and ROS formation (7254.8±385.7 vs. 5825.2±375.9

P<0.01). Meanwhile

improvements in mitochondrial membrane potential (10655.33±331.34 vs. 11129.52±262.35

P<0.05) and ATP level (1.20±0.18 nmol/mg protein vs. 2.53±0.25 nmol/mg protein

P<0.01) were observed by treatment with ginsenosides. Furthermore

ginsenosides could down-regulate CYP2E1 expression (P<0.01) and upregulate PPARα expression (P<0.01) in ethanol-treated cells. Ginsenosides could prevent ethanol-induced hepatocyte steatosis in vitro related to the inhibition of oxidative stress and the improvement of mitochondrial function. In addition

the modulation of CYP2E1 and PPARα expression may also play an important role in the protective effect of ginsenosides against lipid accumulation.

Abstract

respectively. Ethanol exposure resulted in the increase of TG level

lipid accumulation and ROS generation

and the decrease of mitochondrial membrane potential and ATP production in the cells. However

ginsenosides significantly reduced TG content (9.69±0.22 μg/mg protein vs. 4.93±0.49 μg/mg protein

P<0.01)

and ROS formation (7254.8±385.7 vs. 5825.2±375.9

P<0.01). Meanwhile

improvements in mitochondrial membrane potential (10655.33±331.34 vs. 11129.52±262.35

P<0.05) and ATP level (1.20±0.18 nmol/mg protein vs. 2.53±0.25 nmol/mg protein

P<0.01) were observed by treatment with ginsenosides. Furthermore

the modulation of CYP2E1 and PPARα expression may also play an important role in the protective effect of ginsenosides against lipid accumulation.

关键词

Ginsenosideshepatocyte steatosisreactive oxygen speciesmitochondrial functioncytochrome P450 2E1peroxisome proliferator-activated receptor α

Keywords

Ginsenosideshepatocyte steatosisreactive oxygen speciesmitochondrial functioncytochrome P450 2E1peroxisome proliferator-activated receptor α

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