Effects of AC-SDKP administration on the NLRP3 inflammasome complex and blood-spinal cord barrier in experimental spinal cord injury
Ultrastructural Pathology, 2026 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Basım Tarihi: 2026
- Doi Numarası: 10.1080/01913123.2026.2710258
- Dergi Adı: Ultrastructural Pathology
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, BIOSIS, EMBASE, MEDLINE, Academic Search Ultimate (EBSCO), Biomedical Reference Collection: Corporate Edition (EBSCO)
- Anahtar Kelimeler: Blood-spinal cord barrier, central nervous system, inflammation, NLRP3 inflammasome, permeability, spinal cord injury
- Çukurova Üniversitesi Adresli: Evet
Özet
This study investigated the effects of N-acetyl-seryl-aspartyl-lysyl-proline (AC-SDKP) treatment on the NLRP3 inflammasome complex and blood-spinal cord barrier (BSCB) permeability in a rat model of spinal cord injury (SCI). Male Wistar rats were divided into control, sham, and experimental groups, with the experimental group further divided into saline-treated and AC-SDKP-treated subgroups. SCI was induced using extradural clip compression, and AC-SDKP was administered intraperitoneally for 7 days post-injury. Spinal cord tissue samples were evaluated using light and electron microscopy, immunohistochemistry, and qRT-PCR. Biochemical analyses of IL-1β and IL-18 levels in blood and tissue samples were performed. Results showed that AC-SDKP treatment reduced edema, hemorrhage, and cavitation, and supported histological recovery. Immunohistochemistry revealed increased NeuN expression and decreased MMP-9 levels in the treatment group, indicating neuroprotection and reduced inflammation. AC-SDKP treatment also preserved BSCB integrity by increasing occludin, claudin-5, and VE-cadherin expression. Molecular analyses showed that AC-SDKP suppressed NF-κB activity and NLRP3 inflammasome levels, leading to decreased caspase-1, IL-1β, and IL-18 levels in both blood and spinal cord tissue. These findings suggest that AC-SDKP exerts neuroprotective effects by regulating inflammation at the cellular level and preserving BSCB integrity, making it a promising therapeutic agent for reducing secondary tissue damage and supporting recovery following SCI.