摘要
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。
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 odclusion （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.
出处
《中国老年学杂志》
CAS
CSCD
北大核心
2012年第21期4658-4659,共2页
Chinese Journal of Gerontology
基金
国家自然科学基金青年项目(No.31100783
81100953)
国家自然科学基金面上项目(No.31171014)
关键词
糖尿病
脑缺血
自噬
Diabetes
Brain ischemia
Autophagy
