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Background <p>Chronic inflammatory diseases are associated with qualitative and quantitative changes in lipid and lipoprotein metabolism, including high density lipoproteins (HDLs), increasing patients´ susceptibility to atherosclerosis and cardiovascular mortality. Given the liver’s central role in lipoprotein metabolism and systemic inflammation, we aimed to develop and investigate an in vitro model of inflammation-induced hepatic metabolic changes.</p> Methods and Results <p>To better approximate in vivo conditions, where systemic inflammation exposes the liver to a complex environment rich in cytokines and inflammatory mediators, we exposed human hepatocarcinoma HepG2 cells to conditioned media (CM) from THP-1-derived macrophages using phorbol-12-myristate-13-acetate (PMA) and lipopolysaccharide (LPS). The effect of CM on mRNA expression in HepG2 was tested by quantitative real-time PCR or protein expression by Western blot analysis. Even short-term exposure to CM (2–4&#xa0;h) led to a significant change in the mRNA expression of inflammatory genes and several transcription factors (e.g., TNF-α, NF-κB, PPARα, and LRH-1). This change was accompanied by alternations in the expression of lipoprotein-associated genes at different time points (e.g. SAA, LDLr, ApoA1, ABCA1, PON1, and PCSK9). After 24&#xa0;h of exposure, no effect on HepG2 viability was observed.</p> Conclusion <p>In our model, we observed several significant inflammation-induced changes in hepatic lipoprotein metabolism, making it a valuable in vitro system for further mechanistic studies.</p>

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HepG2 cells stimulated by THP-1-conditioned medium: a potential in vitro model of systemic inflammation–induced hepatic alterations

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月6日

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  • Veronika Vyletelová,
  • Marek Bohunčák,
  • Jana Hricovíniová,
  • Gabriela Greifová,
  • Peter Vavrinec,
  • Jakub Krivý,
  • Dimitris Kardassis,
  • Ľudmila Pašková

摘要

Background

Chronic inflammatory diseases are associated with qualitative and quantitative changes in lipid and lipoprotein metabolism, including high density lipoproteins (HDLs), increasing patients´ susceptibility to atherosclerosis and cardiovascular mortality. Given the liver’s central role in lipoprotein metabolism and systemic inflammation, we aimed to develop and investigate an in vitro model of inflammation-induced hepatic metabolic changes.

Methods and Results

To better approximate in vivo conditions, where systemic inflammation exposes the liver to a complex environment rich in cytokines and inflammatory mediators, we exposed human hepatocarcinoma HepG2 cells to conditioned media (CM) from THP-1-derived macrophages using phorbol-12-myristate-13-acetate (PMA) and lipopolysaccharide (LPS). The effect of CM on mRNA expression in HepG2 was tested by quantitative real-time PCR or protein expression by Western blot analysis. Even short-term exposure to CM (2–4 h) led to a significant change in the mRNA expression of inflammatory genes and several transcription factors (e.g., TNF-α, NF-κB, PPARα, and LRH-1). This change was accompanied by alternations in the expression of lipoprotein-associated genes at different time points (e.g. SAA, LDLr, ApoA1, ABCA1, PON1, and PCSK9). After 24 h of exposure, no effect on HepG2 viability was observed.

Conclusion

In our model, we observed several significant inflammation-induced changes in hepatic lipoprotein metabolism, making it a valuable in vitro system for further mechanistic studies.