突触融合蛋白Syntaxin17调节自噬对脑缺血再灌注致神经元凋亡产生保护作用

Objective:The study was aimed to study the neuroprotection of STX17. Methods: Ischemia / reperfusion (I / R) model was established in mice and oxygen glucose deprivation (OGD) modelwas established in primary cortical neurons.Lentivirus was applied to knockdown STX17 protein expression. LC3, P62, caspase3, PARP were detected by Western blot. Cell viability and cytotoxicity were measured by cell counting kit 8and lactate dehydrogenase kit. Autophagic flux, lysosome number, cell morphology and apoptosiswere detected by Immunofluorescence. Results: STX17 was increased after I/R and O/R. Knocking down STX17 would block autophagic flux, increase autophagy-related proteinsLC3, P62, and apoptosis-related proteins caspase 3,PARP. Lysosomal function.and cell viability were also impaired. Conclusion: STX17 affects autophagy and exerts neuroprotection in I/R injury.