Temporal Expression Pattern of Lipid Metabolism-related Genes and Reactive Oxygen Species (ROS) Level in Grass Carp (Ctenopharyngodon idellus) L8824 Cell Line during Hepatic Steatosis

Yang Li, Lian Wu


Objective: To investigate the mechanism of grass carp hepatic steatosis and the role of ROS in this process, grass carp liver cell line L8824 is used to establish the hepatic steatosis model by induction with oleic acid. Methods: The CCK8 kit and alanine transaminase (ALT) and aspartate transaminase (AST) were used to evaluate the cell variability and cell damage. Real time-PCR was used to detect the  key genes of lipid metabolism (PPAR, SREBP-1c, ACC, SCD-1, CPT-1 and MTTP). DCFH-DA probe was used to detect ROS. The results showed that treatment with oleic acid can continuously reduce the cell viability and exacerbate cell damage. The fatty acid de novo synthesis, β-oxidation a temporal expression pattern of lipid metabolism-related genes and Reactive Oxygen Species (ROS) level in grass carp (Ctenopharyngodon idellus) L8824 cell line during hepatic steatosisnd VLDL assemble were enhanced during the treatment from 0-24h, and then all the aspects were impaired by continuous induction. The ROS was maintained at a low level during 0-24h, then significantly increased at 36 h, then decreased to a second high level. Conclusion: The lipogenesis, β-oxidation, and triglyceride (TG) transportation are all heightened during nutritional steatosis until the hepatocytes fully loaded with fat, and the ROS levels perform in an opposite trend.


Aquaculture; Hepatic Steatosis; Lipid Metabolism Related Genes; Reactive Oxygen Species (ROS)

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DU Z. Causes of fatty liver in farmed fish: a review and new perspectives. Journal of Fisheries of China, 2014, 9: 53.

Lu R, Liang X, Sun J, et al. Establishment of lipid metabolism model of grass carp hepatocytes and analysis of lipid metabolism gene expression. Chinese Aquatic Sciences Learning, 2015,22:24-32.

Lu R, Liang X, Sun J, et al. Establishment of a model of grass carp hepatocyte steatosis and analysis of lipid metabolism gene expression. Journal of Fishery Sciences of China, 2015, 22: 24-32.(in Chinese)

Li X, Sun J, Ji H, et al. Effects of fatty acids on lipid accumulation and apoptosis of grass carp hepatocytes in vitro. Aquatic organisms Journal, 2017, 41: 56-64.

Li X, Sun J, Ji H, et al. Influence of fatty acids on lipid accumulation and apoptosis status of grass carp Ctenopharyngodon idellus hepatocyte in vitro. Acta Hydrobiologica Sinica, 2017, 41: 56-64. (in Chinese)

Dowman J K, Tomlinson J, Newsome P. Pathogenesis of non-alcoholic fatty liver disease. QJM: An International Journal of Medicine, 2009, 103: 71-83.

Nassir F, Rector RS, Hammoud G M, Ibdah J A. Pathogenesis and prevention of hepatic steatosis. J Gastroenterology hepatology, 2015, 11: 167.

Teschke R. Hepatotoxicity: Molecular Mechanisms and Pathophysiology. In. Multidisciplinary Digital Publishing Institute, 2019.

Xiao P, Ji H, Zhang B, et al. Effects of silymarin on lipid accumulation in grass carp hepatocytes and its mechanism. Acta Aquatica Sinica, 2017.41: 1301-1310.

Xiao P, Ji H, Zhang B, et al. Inhibitory effect of silymarin on oleic acid-induced lipid accumulation in grass carp (Ctenopharyngodon idellus) hepatocytes in vitro. Acta Hydrobiologica Sinica, 2017, 41: 1301-1310. (in Chinese)

Vernon G, Baranova A, Younossi Z. Systematic review: the epidemiology and natural history of non‐alcoholic fatty liver disease and non‐alcoholic steatohepatitis in adults. Alimentary pharmacology and therapeutics, 2011, 34: 274-285.

He W, Barak Y, Hevener A, et al. Adipose-specific peroxisome proliferator-activated receptor γ knockout causes insulin resistance in fat and liver but not in muscle. J Proceedings of the National Academy of Sciences, 2003, 100: 15712-15717.

Rogue A, Antherieu S, Vluggens, et al. PPAR agonists reduce steatosis in oleic acid-overloaded HepaRG cells. Toxicology and applied pharmacology, 2014, 276: 73-81.

Dossi C G, Tapia G S, Espinosa A, et al. Reversal of high-fat diet-induced hepatic steatosis by n-3 LCPUFA: role of PPAR-α and SREBP-1c. The Journal of nutritional biochemistry, 2014, 25: 977-984.

Matsumoto T, Terai S, Oishi T, Et al. Medaka as a model for human nonalcoholic steatohepatitis. Disease models & mechanisms, 2010, dmm. 002311.

Abu-Elheiga L, Oh W, Kordari P, Wakil S J. Acetyl-CoA carboxylase 2 mutant mice are protected against obesity and diabetes induced by high-fat/high-carbohydrate diets. Proceedings of the National Academy of Sciences, 2003, 100: 10207-10212.

DOI: https://doi.org/10.18686/fsa.v1i2.1316


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