Akademik Veri Yönetim Sistemi
Journal of Biochemical and Molecular Toxicology, cilt.39, sa.12, 2025 (SCI-Expanded, Scopus)
The development of neurological diseases is an important but poorly understood condition around worldwide. Therefore, treatment options remain quite limited. This study looked into how lipopolysaccharide (LPS)-induced neuroinflammation was affected in vivo by the cyclooxygenase (COX) inhibitor 4-methylthiazole derivative compound (MET). A total of 40 male Sprague Dawley rats were separated into five groups. To demonstrate the neuroinflammatory damage induced by LPS and to evaluate the mechanism of action of MET; pro- and anti-inflammatory cytokines, enzymes with inflammatory activity and brain-derived markers were evaluated. The efficacy of the MET compound was also compared with one of the reference drugs, the nonselective COX inhibitor indomethacin (INDO). Biochemical, molecular and histopathological analyses revealed that LPS induced severe neuroinflammation in rat brains. MET compound was observed to suppress neuroinflammation through different pathways. Especially when TNF-α, IL-6 and IL-10 results were compared with INDO, anti-inflammatory activity was found to be high. Our results revealed that MET compound may suppress LPS-induced neuroinflammation via COX enzyme inhibition as well as downregulation of pro-inflammatory cytokines and M1 phenotype microglia.