TRIM14 Knockdown is Associated with Attenuated Sevoflurane-Induced Ferroptosis and Mitochondrial Dysfunction in Hippocampal Neurons.

Sevoflurane (SEV) is widely used in clinical anesthesia, but its exposure is increasingly being linked to neurocognitive dysfunction, particularly in hippocampal neurons. TRIM14, an E3 ubiquitin ligase, is essential for regulating inflammation, apoptosis, and mitochondrial function; however, its involvement in SEV-induced neuronal damage remains unclear. In this study, we investigated the role of TRIM14 in SEV-induced hippocampal neuronal damage, focusing on mitochondrial dysfunction, iron homeostasis, and inflammation. The results show that TRIM14 knockdown significantly increased cell viability, restrained apoptosis, and suppressed inflammatory cytokines in SEV-treated neurons. However, it also alleviated mitochondrial dysfunction, mitigated ferroptosis, and regulated iron homeostasis. Furthermore, silencing TRIM14 suppressed the NF-κB and STAT3 axis. These findings suggest that TRIM14 contributes to SEV-induced neuronal damage.