Objective To evaluate the diabetes on transient ischemia-induced autophagy activity. Methods Streptozotocin( STZ)-induced diabetic mellitus ( DM) mice were subjected to transient common carotid artery occlusion ( CCAO) operation. After the operation, immunoblotting and transmission electron microscopy ( EM) were performed to investigate the microtubule-associated protein light chain 3 ( LC3 ) - II and the accumulation of autophagy-like vacuoles containing electron-dense material. Results Western blot analysis showed that LC3-II conjugate was drastically up-regulated at early stages post ischemia and it lasted for at least 72 h; DM mice demonstrated increased baseline level of LC3-II as comparing to normal mice; DM amplified stroke-induced LC3-II level. Conclusions The modulating neuronal autophagy might be a new therapeutic strategy to treat patients with stroke.%目的 评估糖尿病(DM)短暂性脑缺血引起小鼠脑内自噬活性的改变.方法 腹腔注射链脲佐菌素(STZ)诱导小鼠DM模型,通过短暂性双侧颈总动脉夹闭(CCAO)手术在DM模型上建立脑缺血模型.通过免疫印迹和透射电子显微镜(EM)检测脑内自噬活性.结果 在缺血早期,自噬活性标记物LC3-Ⅱ表达大幅度上调,至少持续72 h.与假手术(Sham)组比较,DM组LC3-Ⅱ表达的基线水平增高.DM加剧了中风诱导的LC3-Ⅱ水平,DM-脑缺血(DM-VO)组的LC3-Ⅱ表达增高最为显著.通过透射电镜观察到,缺血后实验动物神经元大量表达自噬囊泡样物质,以DM-VO组表达最为显著.结论 DM加剧了脑缺血后脑内自噬活性水平的增高,调节脑内自噬可能成为一种防治脑缺血损伤的新途径.
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