ArticleCell division2024
Cilostazol protects against degenerative cervical myelopathy injury and cell pyroptosis via TXNIP-NLRP3 pathway.
Article in Cell division, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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Who cites it
4 citing papers in PubMed, 3 citations in OpenAlex.
- Dysregulation of exosomal miRNAs in A2 astrocytes under oxygen-glucose deprivation is associated with neuronal pyroptosis: a role for miR-139-5p in targeting NLRP3.Journal of orthopaedic surgery and research · 2026Article
- Research Progress on the Pyroptosis Mechanism and Related Active Ingredients of Natural Drugs in Spinal Cord Injury.International journal of general medicine · 2026Review
- Conservative and newer drug treatment for degenerative cervical myelopathy.Journal of clinical orthopaedics and trauma · 2025Article
- Voluntary exercise alleviates ischemic brain injury in mice by modulating mitochondrial dysfunction.Iranian journal of basic medical sciences · 2025Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Degenerative cervical myelopathy (DCM) is one of the most common and serious neurological diseases. Cilostazol has protective effects of anterior horn motor neurons and prevented the cell apoptosis. However, there was no literatures of Cilostazol on DCM. In this study, we established the DCM rat model to detect the effects of Cilostazol. Meanwhile, the neurobehavioral assessments, histopathology changes, inflammatory cytokines, Thioredoxin-interacting protein (TXNIP), NOD‑like receptor pyrin domain containing 3 (NLRP3) and pro-caspase-1 expressions were detected by Basso, Beattie, and Bresnahan score assessment, Hematoxylin and Eosin Staining, Enzyme-linked immunosorbent assay, immunofluorescence and Western blotting, respectively. After treated with Cilostazol, the Basso, Beattie, and Bresnahan (BBB) score, inclined plane test and forelimb grip strength in DCM rats were significantly increased meanwhile the histopathology injury and inflammatory cytokines were decreased. Additionally, TXNIP, NLRP3 and pro-caspase-1 expressions levels were decreased in Cilostazol treated DCM rats. Interestingly, the using of siTXNIP significantly changed inflammatory cytokines, TXNIP, NLRP3 and pro-caspase-1 expressions, however there was no significance between siTXNIP and Cilostazol + siTXNIP group. These observations showed that Cilostazol rescues DCM injury and ameliorates neuronal destruction mediated by TXNIP/NLRP3/caspase-1 and pro-inflammatory cytokines. As a result of our study, these findings provide further evidence that Cilostazol may represent promising therapeutic candidates for DCM.
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