中文摘要：

目的：探讨脑卒中前蛋白去乙酰化酶2（histone deacetylase 2,HDAC2）对于光诱导血栓形成性脑缺血模型小鼠行为学缺陷的作用。方法：通过微量给药系统将腺相关病毒AAV-CAG-EGFP-Cre（2μL）注射至HDAC2flox/flox鼠的运动皮层用以敲减HDAC2,通过免疫荧光以及免疫印迹（Western blot）分析确证病毒AAV-CAG-EGFP-Cre与对照病毒AAV-CAG-EGFP的表达。7 d后进行光诱导血栓形成性脑缺血造模,并于造模前第3天以及造模后第8天采用网格实验和圆筒实验分别检测造模前后AAV-CAG-EGFP-Cre组与AAV-CAG-EGFP组行为学的改变。结果：病毒AAV-CAG-EGFP-Cre相较于对照AAV-CAG-EGFP能特异性地敲减HDAC2,免疫荧光表现为GFP与HDAC2双阳性细胞数减少,Western blot显示针孔周围区HDAC2表达水平降低（P〈0.05）。脑缺血前后的行为学检测表明病毒干预后,HDAC2的下调对缺血前行为学无影响,但显著降低了脑缺血后网格实验的失足率（P〈0.001）与圆筒实验的不对称指数（P〈0.001）,促进了行为学改善。结论：脑卒中前通过重组病毒敲减HDAC2,可以改善脑卒中后小鼠行为学缺陷。

英文摘要：

Objective：To explore the influence of intervention of histone deacetylase 2 （HDAC2） on behavioristics of mice after photothrombotic stroke.Methods：Adeno-associated virus AAV-CAG-EGFP-Cre （2 μL） was microinjected through microcannula to the motor cortex of HDAC2flox/floxmice,aiming to knockdown HDAC2.And then,the expression of virus AAV-CAG-EGFP-Cre and its control AAV-CAG-EGFP was validated through immunofluorescence and Western blot.Seven days later,photothrombotic stroke was induced in the mice,and grid-walking task and cylinder task were conducted at day 3 before stroke and day 8 after stroke to detect behavior changes.Results：Compared with AAV-CAG-EGFP,AAV-CAG-EGFP-Cre significantly down-regulated HDAC2 expression,which was showed in the reduction of the number of GFP＋/HDAC2＋cells and the expression level of HDAC2 in the peri-pinhole zone （P〈0.05）.Behavioral tests demonstrated that the decrease of HDAC2 didn＇t influence the behavior before ischemia,but significantly reduced foot faults in the grid-walking task （P〈0.001） and asymmetry index in the cylinder task （P〈0.001） after ischemia,which improved behavioral deficits.Conclusion：HDAC2 knock down by viral interference can promote functional recovery after photothrombotic stroke.