Karimkhani, HadiShojaolsadati, PariaYigitbasi, TurkanKolbasi, BircanEmekli, NeslinTıbbi Biyokimya / Medical Biochemistry2024-05-252024-05-25202400753-33221950-600710.1016/j.biopha.2024.1165392-s2.0-85190292716https://doi.org/10.1016/j.biopha.2024.116539This study aimed to investigate the effects of the calpain inhibitor N-Acetyl-Leu-Leu-norleucinal (ALLN) on neuroapoptotic cell damage caused by Copper Oxide Nanoparticles (CuO-NP) and exacerbation of damage through brain ischemia/reperfusion (I/R) in a rat model. Male Wistar Albino rats (n=80) were divided into eight groups: Control, I/R, CuO-NP, CuO-NP+I/R, I/R+ALLN, CuO-NP+ALLN, CuO-NP+I/R+ALLN, and DMSO. Biochemical markers (MBP, S100B, NEFL, NSE, BCL-2, Cyt-C, Calpain, TNF-alpha, Caspase-3, MDA, and CAT) were measured in serum and brain tissue samples. Histological examinations (H&E staining), DNA fragmentation analysis (TUNEL) were performed, along with Caspase-3 assessment. The ALLN-treated groups exhibited significant improvements in biochemical markers and a remarkable reduction in apoptosis compared to the damaged groups (CuO-NP and I/R). H&E and Caspase-3 staining revealed damage-related morphological changes and reduced apoptosis in the ALLN-treated group. However, no differences were observed among the groups with TUNEL staining. The findings suggest that ALLN, as a calpain inhibitor, has potential implications for anti-apoptotic treatment, specifically in mitigating neuroapoptotic cell damage caused by CuO-NP and I/R.eninfo:eu-repo/semantics/openAccessCopper oxide nanoparticle (CuO-NP)Brain ischemia-reperfusion (I/R)Cerebral ischemia-reperfusion (I/R)Calpain inhibitorAnti-apoptotic treatmentRat modelArticleQ1Q1174WOS:00122977940000138615610