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Cited by 13Liver Disease Diagnosis and TreatmentLiver physiology and pathologyDrug-Induced Hepatotoxicity and Protection

Oxidative Stress and Annexin A2 Differential Expression in Free Fatty Acids-Induced Non-Alcoholic Fatty Liver Disease in HepG2 Cells

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Arruda, Vinícius Marques, Azevedo, Gabriela Tolentino, Granato, Maria Júlia Maia Gonçalves, Matos, André Carlos Pereira, Araújo, Thaise Gonçalves, Guerra, Joyce Ferreira da Costa·2024·International Journal of Molecular Sciences
DOI 10.3390/ijms25179591PMC PMC11395542
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Abstract

Non-alcoholic fatty liver disease (NAFLD) is a rising global burden, affecting one in four adults. Despite the increasing prevalence of NAFLD, the exact cellular and molecular mechanisms remain unclear, and effective therapeutic strategies are still limited. In vitro models of NAFLD are critical to understanding the pathogenesis and searching for effective therapies; thus, we evaluated the effects of free fatty acids (FFAs) on NAFLD hallmarks and their association with the modulation of Annexin A2 (ANXA2) and Keratin 17 (KRT17) in HepG2 cells. Our results show that oleic and palmitic acids can differentially induce intracellular lipid accumulation, cell death, and promote oxidative stress by increasing lipid peroxidation, protein carbonylation, and antioxidant defense depletion. Moreover, a markedly increased expression of inflammatory cytokines demonstrated the activation of inflammation pathways associated with lipotoxicity and oxidative stress. ANXA2 overexpression and KRT17 nuclear translocation were also observed, supporting the role of both molecules in the progression of liver disease. Taken together, these data provide insights into the interplay between ANXA2 and KRT17 in NAFLD, paving the way for understanding molecular mechanisms involved with the disease and developing new therapeutic strategies.

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  • The range of 0.1 to 2.0 mM for the combination of FAs is the standard range for modeling MASLD in 2D HepG2 monoculture.

    “The range of 0.1 to 2.0 mM for the combination of FAs is the standard range for modeling MASLD in 2D HepG2 monoculture [93,100,125,126,127,128].”

    From The HepG2 Cell Line as a Model for Studying Metabolic Dysfunction-Associated Steatotic Liver Disease (2026) · cites this paper as [125]

    The Introduction says there is little consensus on experimental standardization, contrary to calling 0.1–2.0 mM a standard range. The Discussion instead describes concentrations of 0.3–3 mM in most in vitro studies. Although this paper uses combined fatty acids at 1 and 2 mM in HepG2 cells (Materials and Methods, §4.3), it does not establish the claimed range as standard. (LLM, conf=0.85)

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  • To induce steatosis in HepG2, supraphysiological concentrations of FFAs (0.5-2.0 mM) are often used.

    “Second, to induce steatosis, supraphysiological concentrations of FFAs (concentrations of 0.5–2.0 mM) are often used in HepG2 experiments [28,91,125,126,127,128,129,130].”

    From The HepG2 Cell Line as a Model for Studying Metabolic Dysfunction-Associated Steatotic Liver Disease (2026) · cites this paper as [125]

    Materials and Methods §4.3 reports using 0.7, 1, and 2 mM FFAs in HepG2 cells, and Results §2.1 reports that these treatments induced lipid accumulation. The paper does not establish that the full 0.5–2.0 mM range is often used or describe those concentrations as supraphysiological. Page numbers were not available in our copy. (LLM, conf=0.85)

    Experimental — accuracy not yet measured

  • In subsequent studies, in vitro modeling of liver steatosis in HepG2 was performed by incubating cells with a mixture of free fatty acids, most often OA and PA, in a molar ratio of 1:1 or 2:1, at a total concentration of 0.5 to 1 mM, for 24-48 h.

    “In subsequent studies, in vitro modeling of liver steatosis in the HepG2 cell line was performed by incubating cells with a mixture of free fatty acids, most often OA and PA, in a molar ratio of 1:1 or 2:1, at a total concentration of 0.5 to 1 mM, for 24–48 h [28,125].”

    From The HepG2 Cell Line as a Model for Studying Metabolic Dysfunction-Associated Steatotic Liver Disease (2026) · cites this paper as [125]

    Materials and Methods §4.3 (page not provided) describes HepG2 steatosis induced with oleic and palmitic acids at a 2:1 ratio for 24 or 48 hours. Its combined-FFA concentrations were 1 and 2 mM, not the claimed range of 0.5–1 mM; it does not describe a 1:1 ratio. The Introduction notes little consensus on experimental standardization, so this paper also does not establish that the claimed conditions were used most often across studies. (LLM, conf=0.89)

    Experimental — accuracy not yet measured

  • Incubation with a mixture OA + PA in a 2:1 ratio at high FFA concentrations (1-2 mM for 24-48 h) caused more pronounced lipid accumulation, increased markers of oxidative damage, and a significant rise in IL-1β, IL-6, IL-17, IL-22, and TGF-β; however, 48 h exposure did not result in a proportional increase in steatosis and was accompanied by a significant decrease in cell viability.

    “Arruda et al. demonstrated that incubation with a mixture OA + PA in a 2:1 ratio (under exposure to high FFA concentrations—1–2 mM for 24–48 h) caused more pronounced lipid accumulation, increased markers of oxidative damage, and a significant rise in IL-1β, IL-6, IL-17, IL-22, and TGF-β. However, it should be noted that 48 h exposure did not result in a proportional increase in steatosis; under”

    From The HepG2 Cell Line as a Model for Studying Metabolic Dysfunction-Associated Steatotic Liver Disease (2026) · cites this paper as [125]

    Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

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  • Concentrations of approximately 1-2 mM, especially with exposure of 48 h or more, promote lipotoxicity to a greater extent.

    “Consequently, concentrations of approximately 1–2 mM, especially with exposure of 48 h or more, promote lipotoxicity to a greater extent [125].”

    From The HepG2 Cell Line as a Model for Studying Metabolic Dysfunction-Associated Steatotic Liver Disease (2026) · cites this paper as [125]

    The Methods (§4.3; page unavailable) specify 1 and 2 mM oleic–palmitic acid mixtures, and the Results (§2.1; page unavailable) report greater cytotoxicity at 48 h than at 24 h in HepG2 cells. The paper tested only those two exposure durations, so it does not establish the claim for exposures longer than 48 h or for fatty acids generally. (LLM, conf=0.86)

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Authors
Arruda, V. M., Azevedo, G. T., Granato, M. J. M. G., Matos, A. C. P., Araújo, T. G., & Guerra, J. F. D. C.
Affiliations
Universidade Federal de Uberlândia (BR)
Corresponding author
Guerra, Joyce Ferreira da Costa
ORCID
Venue
International Journal of Molecular Sciences
Publisher
MDPI AG
Published
2024-09-04
Volume
25
Issue
17
Pages
9591
ISSN
1422-0067 (ISSN-L)
DOI
10.3390/ijms25179591
PMC
PMC11395542
OpenAlex
W4402230244
Cited by
13
References
54
Citations by year
2026: 8 · 2025: 5
FWCI
3.97
Type
journal article
Language
en
Open access
Licence
Locations
  • International Journal of Molecular Sciences (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Funders
  • Fundação de Amparo à Pesquisa do Estado de Minas Gerais (FAPEMIG) (APQ-01564-18, APQ-00760-18, INCT-TeraNano—CNPq #403193/2022-2, FAPEMIG CBB—APQ-03613-17)
  • Fundação Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) (APQ-01564-18, APQ-00760-18, INCT-TeraNano—CNPq #403193/2022-2, FAPEMIG CBB—APQ-03613-17)
  • Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) (APQ-01564-18, APQ-00760-18, INCT-TeraNano—CNPq #403193/2022-2, FAPEMIG CBB—APQ-03613-17)
  • National Institute of Science and Technology in Theranostics and Nanobiotechnology (APQ-01564-18, APQ-00760-18, INCT-TeraNano—CNPq #403193/2022-2, FAPEMIG CBB—APQ-03613-17)
Topics
  • Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
  • Health Sciences › Medicine › Hepatology › Liver physiology and pathology
  • Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Drug-Induced Hepatotoxicity and Protection
Keywords
non-alcoholic fatty liver disease, free fatty acids, oleic acid, palmitic acid, annexin A2, keratin 17, oxidative stress, lipid peroxidation, protein carbonylation, antioxidant defense, lipid accumulation, hepatocyte death, inflammatory cytokines, lipotoxicity, HepG2 cells, nuclear translocation
MeSH terms
Fatty Acids, Nonesterified, Humans, Lipid Peroxidation, Annexin A2, Oxidative Stress, Lipid Metabolism, Hep G2 Cells, Non-alcoholic Fatty Liver Disease

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