Journal
BIOCHEMICAL PHARMACOLOGY
Volume 210, Issue -, Pages -Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.bcp.2023.115457
Keywords
Noise-induced hearing loss; Oridonin; Interleukin 1 receptor type 2; Inflammasome; Inflammation; Interleukin 1 receptor type 1
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Using RNA sequencing analysis, this study found that the traditional medicine oridonin (Ori) may protect against noise-induced hearing loss (NIHL) by regulating the expression of interleukin 1 receptor type 2 (IL1R2). Overexpression of IL1R2 in the inner ears of mice significantly reduced noise-induced ribbon synapse lesions and hearing loss by blocking the cytokine storm. This study provides a novel theoretical foundation for guiding the clinical treatment of NIHL.
NOD-like receptor protein 3 (NLRP3) inflammasomes trigger the inflammatory cascades and participate in various inflammatory diseases, including noise-induced hearing loss (NIHL) caused by oxidative stress. Recently, the anti-inflammatory traditional medicine oridonin (Ori) has been reported to provide hearing protection in mice after noise exposure by blocking the NLRP3-never in mitosis gene A-related kinase 7 (NEK7)-inflammasome complex assembly. Using RNA sequencing analysis, we further elucidated that interleukin 1 receptor type 2 (IL1R2) may be another crucial factor regulated by Ori to protect NIHL. We observed that IL1R2 expression was localized in spiral ganglion neurons, inner and outer hair cells, in Ori-treated mouse cochleae. Additionally, we confirmed that ectopic overexpression of IL1R2 in the inner ears of healthy mice using an adeno-associated virus delivery system significantly reduced noise-induced ribbon synapse lesions and hearing loss by blocking the cytokine storm in the inner ear. This study provides a novel theoretical foundation for guiding the clinical treatment of NIHL.
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