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<p>Cisplatin is a broad-spectrum anticancer agent. Its main side effect - ototoxicity - may impact the quality of patient’s life. Eleutheroside E (EE), the main active component of <i>Acanthopanax</i>, exhibits antioxidant and anti-inflammatory properties. This study investigates the protective effects of EE against cisplatin-induced ototoxicity and its underlying mechanisms. We use <i>C57BL/6 J</i> mice, the House Ear Institute-Organ of Corti 1 (HEI-OC1) cells, and cultured cochlear basement membranes in our experiments. We employ network pharmacology and 4D-FastDIA quantitative proteomic analysis. Our results demonstrate that Cisplatin significantly impairs auditory function in mice. However, EE co-treatment preserves auditory function across most measured frequencies, correlating with reduced damage to cochlear hair cells and spiral ganglion neurons(SGNs). Here, we show that EE attenuates cisplatin-induced pro-inflammatory responses and cellular pyroptosis, possibly via downregulation of the MAPK/NF-κB/NLRP3 signaling pathway. In conclusion, EE may offer a promising strategy for reducing Cisplatin’s ototoxicity without affecting its antitumor efficacy.</p><p></p>

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Eleutheroside E alleviates cisplatin-induced ototoxicity by down-regulating MAPK/NF-κB/NLRP3 signaling pathway and inhibiting cochlear cell pyroptosis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月8日

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  • Ya’nan Zhang,
  • Ling Lu,
  • Busheng Tong,
  • Jingjing Wang,
  • Kunjian Liu,
  • Jialiang Zhang,
  • Di Zhang,
  • Meihui Tian,
  • Weifang Sun,
  • Huan Liu,
  • Ping Wang,
  • Maoli Duan,
  • Yong Tang

摘要

Cisplatin is a broad-spectrum anticancer agent. Its main side effect - ototoxicity - may impact the quality of patient’s life. Eleutheroside E (EE), the main active component of Acanthopanax, exhibits antioxidant and anti-inflammatory properties. This study investigates the protective effects of EE against cisplatin-induced ototoxicity and its underlying mechanisms. We use C57BL/6 J mice, the House Ear Institute-Organ of Corti 1 (HEI-OC1) cells, and cultured cochlear basement membranes in our experiments. We employ network pharmacology and 4D-FastDIA quantitative proteomic analysis. Our results demonstrate that Cisplatin significantly impairs auditory function in mice. However, EE co-treatment preserves auditory function across most measured frequencies, correlating with reduced damage to cochlear hair cells and spiral ganglion neurons(SGNs). Here, we show that EE attenuates cisplatin-induced pro-inflammatory responses and cellular pyroptosis, possibly via downregulation of the MAPK/NF-κB/NLRP3 signaling pathway. In conclusion, EE may offer a promising strategy for reducing Cisplatin’s ototoxicity without affecting its antitumor efficacy.