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Background <p>Age-related hearing loss (ARHL) is closely linked to chronic inflammation and cellular senescence, with NF-κB signaling playing a key role in promoting inflammatory responses and driving senescence. While IL-37 is known for its anti-inflammatory effects, its potential to modulate NF-κB and attenuate senescence in auditory cells remains unclear. This study investigates whether IL-37 protects against cellular senescence in HEI-OC1 cells by regulating NF-κB signaling.</p> Objective <p>To evaluate the protective functions of IL-37 in senescent HEI-OC1 cochlear hair cells and explore its underlying regulatory mechanisms.</p> Methods <p>HEI-OC1 cochlear hair cells were induced to undergo senescence using <span>d</span>-galactose (<span>D</span>-gal) and then treated with recombinant human IL-37 (rhIL-37) or the NF-κB inhibitor PDTC (pyrrolidine dithiocarbamoyl trimethoprim). The study included four experimental groups: normal control, D-gal-induced senescence (D-gal-senescence), rhIL-37 treatment, and PDTC treatment. Cellular proliferation, senescence markers, inflammatory cytokine levels, NF-κB pathway-associated proteins, nuclear translocation of NF-κB p65, as well as apoptotic factor expression were analyzed.</p> Results <p>D-gal was found to effectively induce senescence in HEI-OC1 cells. IL-37 treatment improved cell viability, reduced pro-apoptotic factors Caspase-3 and pro-inflammatory cytokines (IL-6, IL-1β, and TNF-α), as well as reducing HEI-OC1 cell senescence following D-gal treatment. Here, analysis of the NF-κB pathway indicated reduced nuclear translocation of NF-κB p65 and reduced phosphorylation with IL-37 treatment, demonstrating similar effects of PDTC-mediated NF-κB inhibition.</p> Conclusion <p>IL-37 reduces inflammation and apoptotic damage while attenuating D-gal-mediated HEI-OC1 cell senescence, possibly by downregulating NF-κB pathway activation.</p>

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IL-37 attenuates HEI-OC1 cell senescence by modulating the NF-κB pathway

  • 期刊论文

  • 发表日期：

    2025年12月29日

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  • Luan Xu,
  • Beibei Xu,
  • Liya Ding,
  • Shumin Li,
  • Xiaopei Wu,
  • Guanghui Wang,
  • Yuefeng Han

摘要

Background

Age-related hearing loss (ARHL) is closely linked to chronic inflammation and cellular senescence, with NF-κB signaling playing a key role in promoting inflammatory responses and driving senescence. While IL-37 is known for its anti-inflammatory effects, its potential to modulate NF-κB and attenuate senescence in auditory cells remains unclear. This study investigates whether IL-37 protects against cellular senescence in HEI-OC1 cells by regulating NF-κB signaling.

Objective

To evaluate the protective functions of IL-37 in senescent HEI-OC1 cochlear hair cells and explore its underlying regulatory mechanisms.

Methods

HEI-OC1 cochlear hair cells were induced to undergo senescence using d-galactose (D-gal) and then treated with recombinant human IL-37 (rhIL-37) or the NF-κB inhibitor PDTC (pyrrolidine dithiocarbamoyl trimethoprim). The study included four experimental groups: normal control, D-gal-induced senescence (D-gal-senescence), rhIL-37 treatment, and PDTC treatment. Cellular proliferation, senescence markers, inflammatory cytokine levels, NF-κB pathway-associated proteins, nuclear translocation of NF-κB p65, as well as apoptotic factor expression were analyzed.

Results

D-gal was found to effectively induce senescence in HEI-OC1 cells. IL-37 treatment improved cell viability, reduced pro-apoptotic factors Caspase-3 and pro-inflammatory cytokines (IL-6, IL-1β, and TNF-α), as well as reducing HEI-OC1 cell senescence following D-gal treatment. Here, analysis of the NF-κB pathway indicated reduced nuclear translocation of NF-κB p65 and reduced phosphorylation with IL-37 treatment, demonstrating similar effects of PDTC-mediated NF-κB inhibition.

Conclusion

IL-37 reduces inflammation and apoptotic damage while attenuating D-gal-mediated HEI-OC1 cell senescence, possibly by downregulating NF-κB pathway activation.