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Chemerin/CMKLR1 pathway exacerbates cisplatin-induced spiral ganglion neuron injury

  • Jie Tian (Department of Otology, Zibo Central Hospital) ;
  • Ying Mu (Department of Emergency Medicine, Zibo Central Hospital) ;
  • Lili Ma (Department of Neurology, Zibo Central Hospital)
  • Received : 2023.01.31
  • Accepted : 2023.08.02
  • Published : 2024.01.15

Abstract

This study investigated whether chemerin/chemokine-like receptor 1 (CMKLR1) pathway participate in cisplatin-induced spiral ganglion neuron (SGN) damage. Middle cochlear turn was collected from C57BL/6 mice and the SGNs were cultured. Cisplatin, 2-(anaphthoyl) ethyltrimethylammonium iodide (α-NETA), or recombinant mouse chemerin was added into the medium for the treatment. Relative mRNA and protein expression was determined by RT-PCR, ELISA and Western blot, respectively. In cultured mouse cochlear SGNs, the treatment of cisplatin enhanced the secretion of chemerin and CMKLR1. Recombinant chemerin promoted but α-NETA inhibited chemerin/CMKLR1 pathway in cisplatin stimulated SGNs. Cisplatin-induced apoptosis and inflammation response in SGNs were enhanced by recombinant chemerin while inhibited by α-NETA. Recombinant chemerin promoted but α-NETA inhibited NF-κB signal in cisplatin stimulated SGNs. In conclusion, chemerin/CMKLR1 pathway regulated apoptosis and inflammation response in cisplatin-induced SGN injury through NF-κB signaling pathway.

Keywords

References

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