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
首发时间:2018-10-16
摘要:目的:研究STX17的神经保护作用。方法:分别建立小鼠缺血再灌注模型(I/R)和原代皮层神经元氧糖剥夺模型(OGD)。利用慢病毒敲低STX17蛋白表达.。免疫印迹检测LC3,P62,caspase3,PARP蛋白。利用细胞计数试剂盒和乳酸脱氢酶试剂盒检测细胞活力和细胞毒性。免疫荧光检测自噬流,溶酶体数量以及观察细胞形态和凋亡。结果:缺血再灌注引起STX17表达升高。敲低STX17导致自噬流阻滞,LC3,P62堆积,溶酶体功能受损。细胞活力下降,凋亡蛋白表达增多。结论:STX17影响自噬并发挥神经保护作用。
关键词: STX17 氧糖剥夺 自噬 原代皮层神经元 神经保护作用
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STX17 Regulates Autophagy and Protects Neurons from Apoptosis Induced by Iscemia/Reperfusion
Abstract: 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.
Keywords: STX17 Oxygenglucose deprivation Autophagy Cortical neurons Neuroprotection
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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
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