Open Access
ARTICLE
Protective effects of docosahexaenoic acid against non-alcoholic hepatic steatosis through activating of JAK2/STAT3 signaling pathway
YUE WANG1,#, YINPING DUAN1,#, KUNLIN CHEN3, HUIXIA LI1,2,*, YAN QUAN4,*
1 College of Animal Science and Technology, Nanjing Agricultural University, Nanjing, 210095, China
2 Nanjing XinRuize Agricultural Biotechnology Co., Ltd., Nanjing, 210095, China
3 Jiangsu Key Laboratory for Food Quality and Safety-State Key Laboratory Cultivation Base, Ministry of Science and Technology, Jiangsu Academy of Agricultural Sciences, Nanjing, 210014, China
4 College of Pharmacy, Shaanxi University of Chinese Medicine, Xianyang, 712046, China
* Address correspondence to: Huixia Li, ; Yan Quan,
# These authors contributed equally
BIOCELL 2021, 45(2), 307-316. https://doi.org/10.32604/biocell.2021.014305
Received 16 September 2020; Accepted 24 November 2020; Issue published 19 February 2021
Abstract
Non-alcoholic fatty liver disease is the most common cause of hepatic dysfunction. In the present study, human
normal hepatocyte L02 cells were treated with 50% fetal bovine serum to induce the formation of hepatic steatosis
in vitro,
and then the cells were treated with docosahexaenoic acid to investigate its protective effect on Non-alcoholic fatty liver
disease. Our results showed that 50% of fetal bovine serum significantly induced intracellular lipid accumulation and
hepatocyte fatty degeneration within 48 h. The expression level of adipose formation-related genes was significantly
up-regulated, such as PPARγ, C/EBPα and SREBP-1; meanwhile, the content of cellular total lipid, total cholesterol
and triglycerides were significantly increased after 50% fetal bovine serum treatment. Interestingly, docosahexaenoic
acid treatment could inhibit FBS-induced intracellular lipid accumulation in L02 cells and the expression of lipogenic
genes. Moreover, docosahexaenoic acid treatment could reduce hepatic steatosis-induced oxidative stress and
endoplasmic reticulum stress response, and these responses were shown by the modification of antioxidant enzyme
activities and GRP78, CHOP expression. In addition, the results showed that docosahexaenoic acid can activate the
JAK2/STAT3 signaling pathway in fatty liver L02 cell; inhibition of JAK2/STAT3 signaling pathway by WP1066
abolished the beneficial effects of docosahexaenoic acid on hepatic steatosis accompanied with the increased
expression of lipogenic genes and endoplasmic reticulum stress response. Above all, the present study showed that
docosahexaenoic acid can alleviate non-alcoholic hepatic steatosis by activating JAK2/STAT3 signaling pathway.
Keywords
Cite This Article
WANG, Y., DUAN, Y., CHEN, K., LI, H., QUAN, Y. (2021). Protective effects of docosahexaenoic acid against non-alcoholic hepatic steatosis through activating of JAK2/STAT3 signaling pathway.
BIOCELL, 45(2), 307–316.