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Purpose <p>To evaluate the combined effects of empagliflozin (EMPA) and curcumin (Cur) on hepatic macrophage polarization, cytokine profile, and NF-κB signaling in a mouse model of metabolic dysfunction-associated steatotic liver disease (MASLD).</p> Methods <p>Male C57BL/6J mice (<i>n</i> = 10/group) were fed NCD, HFD, HFD+EMPA, HFD + Cur, or HFD+EMPA + Cur for 23 weeks. Hepatic macrophage infiltration (F4/80 immunofluorescence), M1/M2 polarization markers (CD11c, CD206, Arg-1), cytokine levels (TNF-α, IL-6, IL-1β, IL-10), NF-κB p65 expression (Western blot), and histopathology (H&amp;E) were assessed.</p> Results <p>HFD induced macrophage infiltration, predominant M1 polarization, increased pro-inflammatory cytokine levels, and upregulation of NF-κB p65. Both EMPA and Cur monotherapies partially attenuated these changes. Co-administration produced the most pronounced effects: significantly reducing macrophage infiltration (<i>p</i> &lt; 0.001), suppressing CD11c (<i>p</i> &lt; 0.001), restoring CD206 and Arg-1 (<i>p</i> &lt; 0.01 for both), markedly reducing TNF-α, IL-6, and IL-1β (<i>p</i> &lt; 0.001 for all), elevating IL-10 (<i>p</i> &lt; 0.001), and suppressing total NF-κB p65 protein expression (<i>p</i> &lt; 0.001).</p> Conclusion <p>Co-administration of EMPA and Cur attenuates HFD-induced hepatic inflammation by remodeling macrophage polarization from M1 toward the M2 phenotype and attenuating NF-κB-associated inflammatory signaling, as reflected by reduced total p65 protein expression, with effects more pronounced than either agent alone.</p>

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Combination of empagliflozin with curcumin attenuates hepatic inflammation in high-fat diet-fed mice via macrophage polarization remodeling and NF-κB modulation

  • 期刊论文

  • 发表日期：

    2026年7月13日

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  • Masoume Aliabadi,
  • Ali Akbar Soleimani,
  • Gholamreza Taheripak,
  • Mitra Nourbakhsh,
  • Reza Meshkani

摘要

Purpose

To evaluate the combined effects of empagliflozin (EMPA) and curcumin (Cur) on hepatic macrophage polarization, cytokine profile, and NF-κB signaling in a mouse model of metabolic dysfunction-associated steatotic liver disease (MASLD).

Methods

Male C57BL/6J mice (n = 10/group) were fed NCD, HFD, HFD+EMPA, HFD + Cur, or HFD+EMPA + Cur for 23 weeks. Hepatic macrophage infiltration (F4/80 immunofluorescence), M1/M2 polarization markers (CD11c, CD206, Arg-1), cytokine levels (TNF-α, IL-6, IL-1β, IL-10), NF-κB p65 expression (Western blot), and histopathology (H&E) were assessed.

Results

HFD induced macrophage infiltration, predominant M1 polarization, increased pro-inflammatory cytokine levels, and upregulation of NF-κB p65. Both EMPA and Cur monotherapies partially attenuated these changes. Co-administration produced the most pronounced effects: significantly reducing macrophage infiltration (p < 0.001), suppressing CD11c (p < 0.001), restoring CD206 and Arg-1 (p < 0.01 for both), markedly reducing TNF-α, IL-6, and IL-1β (p < 0.001 for all), elevating IL-10 (p < 0.001), and suppressing total NF-κB p65 protein expression (p < 0.001).

Conclusion

Co-administration of EMPA and Cur attenuates HFD-induced hepatic inflammation by remodeling macrophage polarization from M1 toward the M2 phenotype and attenuating NF-κB-associated inflammatory signaling, as reflected by reduced total p65 protein expression, with effects more pronounced than either agent alone.