ArticleInternational journal of medical sciences2025
Exosomes derived from TNF-α preconditioned bone marrow mesenchymal stem cells alleviate cisplatin-induced ototoxicity in mice.
Article in International journal of medical sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Efficacy and Safety of Rb-bFGF in Hair Transplantation: A Prospective and Comparative Study.Journal of cosmetic dermatology · 2025Trial
- Adipose-Derived Mesenchymal Stem Cell Exosomes Attenuate Oxygen-Glucose Deprivation-Induced Cochlear Damage by Inducing Autophagy-Associated Signaling.International journal of molecular sciences · 2026Article
- Human adipose stem cell-derived exosomes modulate the transcriptome of D-galactose-Induced neuronal cells.Scientific reports · 2026Article
- Engineered Exosomes: Advances in Therapeutic Applications for Otolaryngology-Head and Neck Diseases.International journal of nanomedicine · 2026Review
- A Nanomedicine Strategy: Spatiotemporally Programmed Delivery of Engineered Exosomes via Smart Scaffolds for Craniofacial Bone Regeneration.International journal of nanomedicine · 2026Review
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Authors and funding
5 authors.
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Abstract
The polarization of microglia promotes the development of cisplatin-induced ototoxicity, and exosomes (Exo) derived from TNF-α preconditioned mesenchymal stem cells (MSCs) may induce the polarization of macrophage. Mice were intraperitoneally injected with cisplatin to establish the ototoxicity model. Bone marrow MSCs (BMSCs) were preconditioned with TNF-α for 48 h, and the relevant TNF-Exo or Exo was enriched, which were further trans-tympanically administered in the left ear of ototoxic mice. Auditory sensitivity was revealed with auditory brainstem response (ABR) at 8, 16, 24, and 32 kHz. The number of hair cells was detected with Myosin 7a staining. Damaged auditory sensitivity and up-regulated hair cell loss were revealed in cisplatin-exposed mice, which could be reversed by Exo or TNF-Exo treatment. Mechanically, up-regulated Iba1, Cd86, iNOS, Cd206, and Arg1 were detected in cisplatin-exposed cochlea. TNF-Exo or Exo administration further decreased Iba1, Cd86, and iNOS expression, and increased cd206 and Arg1 expression. TNF-Exo or Exo administration inhibited the productin of pro-inflammatory cytokines (IL-1β and IL-6), while enhanced the anti-inflammatory cytokine IL-10 production in the cisplatin-exposed cochlea. Importantly, TNF-Exo administration showed more profound benefits compared with Exo. TNF-α preconditioning might be a new therapeutic option to enhance the capability of BMSCs-derived exosomes against cisplatin-induced ototoxicity.
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