Spexin Attenuates Cerebral Ischemia–Reperfusion–Induced Brain Injury in Rats via Suppression of NF-κB-Associated Inflammation and Apoptosis
Molecular Neurobiology, cilt.63, sa.1, 2026 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 63 Sayı: 1
- Basım Tarihi: 2026
- Doi Numarası: 10.1007/s12035-026-06158-3
- Dergi Adı: Molecular Neurobiology
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, BIOSIS, Chemical Abstracts Core, EMBASE, MEDLINE, Natural Science Collection (ProQuest), Biological Science Database (ProQuest), Biomedical Reference Collection: Corporate Edition (EBSCO), Health Research Premium Collection (ProQuest), Pharma Collection (ProQuest)
- Anahtar Kelimeler: Spexin, Cerebral ischemia-reperfusion, Neuroinflammation, Oxidative stress, Apoptosis, NF-kappa B
- Atatürk Üniversitesi Adresli: Evet
Özet
Cerebral ischemia–reperfusion (I/R) injury continues to be a significant factor contributing to neuronal loss and functional deficits subsequent to ischemic stroke, predominantly driven by oxidative stress, neuroinflammation, and apoptosis. Spexin (SPX), a recently discovered neuropeptide, has emerged as a potential regulator of oxidative and inflammatory mechanisms; however, its role in cerebral I/R injury remains to be elucidated. This study investigated the neuroprotective effects of spexin in a rat model of cerebral I/R injury. Male Wistar rats were randomly assigned to the control, I/R, and I/R+SPX (50 µg/kg, subcutaneously) groups. Ischemia was induced by bilateral common carotid artery occlusion for 30 min followed by 24 h of reperfusion. Neurological, histological, and biochemical parameters were evaluated. I/R injury caused significant neuronal degeneration and necrosis in the prefrontal cortex (p < 0.001), along with increased lipid peroxidation, reduced glutathione levels (p < 0.001), and elevations in TNF-α and IL-6 levels (p < 0.05–0.001). These changes were associated with pronounced expression of NF-κB signaling and increased expression of the pro-apoptotic markers and Caspase-3 (p < 0.001). Spexin administration significantly attenuated neuronal damage, reduced MDA and proinflammatory cytokine levels, restored antioxidant capacity, and suppressed NF-κB immunoreactivity and apoptotic signaling (p < 0.05–0.001). These findings demonstrate that spexin attenuates cerebral I/R–induced brain injury by suppressing oxidative stress, NF-κB-associated inflammation, and apoptosis. Spexin may represent a promising therapeutic candidate for ischemic stroke–associated neuronal injury.