Akademik Veri Yönetim Sistemi
49th FEBS congress, İstanbul, Türkiye, 5 - 09 Temmuz 2025, cilt.15, ss.458-459, (Özet Bildiri)
Microglia are the myeloid lineage cells that play important roles in homeostasis, inflammatory responses, and tissue repair in the brain. Microglial activation plays a central role in neuroinflammation which is associated with neurodegenerative diseases. Tumor necrosis factor-α-induced protein 8-like 2 (TIPE2), a member of the TNFAIP8 family, maintains immune homeostasis and is an important negative regulator of inflammation. Flavonoids are naturally occurring polyphenolic compounds that are known to have neuroprotective effects. Casticin is a polymethoxyflavone which has been shown to have anticancer, antioxidant, and anti-inflammatory activities. In this study, we aimed to investigate the effect of casticin on TIPE2 expression in the lipopolysaccharide (LPS)-stimulated microglial cells in vitro. N9 mouse microglial cells were treated with 0.1, 0.5, and 1 μM of casticin for 24 h, and cell viability was analyzed using WST-1 assay. N9 cells were pretreated with 0.1 and 0.5 μM of casticin for 1 h and then incubated with 1 μg/mL of LPS. TIPE2 mRNA expression was analyzed by qPCR, and protein expression was examined by western blotting. 0.1 and 0.5 μM of casticin had no effect on cell viability, whereas 1 μM of casticin reduced viability. TIPE2 mRNA expression levels decreased at 3, 6, and 24 h after LPS incubation. 0.5 μM of casticin increased LPS-induced decreases in TIPE2 mRNA levels at 24 h. TIPE2 protein expression levels also decreased at 2, 4, 8, and 24 h after LPS incubation. 0.5 μM of casticin increased LPS-induced decreases in TIPE2 protein levels at 24 h. Our results demonstrated that casticin could modulate inflammation by increasing TIPE2 expression in microglial cells, suggesting its neuroprotective potential in neuroinflammation.