摘要
目的观察前列腺素E1对右侧大脑中动脉皮层支闭塞(middle cerebral artery occlusion,MCAO)大鼠内源性神经干细胞增殖和迁移的影响。方法36只大鼠随机分为前列腺素E1(10μg.kg-1·d-1)组,溶剂对照组和假手术组,每组12只。3组大鼠均腹腔注射5-溴脱氧尿嘧啶核苷(5-bromo-2'-deoxyuridine,BrdU)以标记脑内新增殖细胞,并于MCAO术后7d、14d行神经功能评分后处死,测脑梗死体积,观察梗死同侧侧脑室室管膜下区(subventricular zone,SVZ)BrdU+细胞、BrdU+/doublecortin(DCX)+细胞表达、梗死灶周BrdU+细胞表达及SVZ区BrdU+/DCX+细胞的迁移距离。结果MCAO术后7d、14d,与溶剂对照组及假手术组相比,前列腺素E1治疗增加了梗死侧SVZ区BrdU+细胞(7 d:380.3±14.3 vs.251.3±9.5 vs.50.3±5.4;14 d:230.2±10.1 vs.126.2±8.8 vs.24.3±6.3,P<0.05)、BrdU+/DCX+细胞(7 d:209.0±19.6 vs.109.8±14.4 vs.27.3±5.9;14 d:96.2±13.0 vs.47.3±6.8 vs.25.7±6.2,P<0.05)和梗死灶周皮质BrdU+细胞(7 d:349.7±9.2 vs.203.5±12.2 vs.53.8±8.4;14 d:203.4±13.3 vs.136.7±11.8vs.27.2±6.2,P<0.05)表达;术后7 d,前列腺素E1组梗死侧SVZ区BrdU+/DCX+细胞迁移距离比溶剂对照组更远(6039.3μm±1035.6μm vs.3591.5μm±716.6μm,P<0.05);前列腺素E1组与溶剂对照组比较,脑梗死后神经功能评分改善[7 d:1.5(1.0,2.0)vs.2.0(2.0,3.0);14 d:0.5(0,1.0)vs.1.0(1.0,2.0),P<0.05]。结论前列腺素E1可促进大鼠脑梗死后梗死侧SVZ区内源性神经干细胞增殖、迁移和神经功能康复。
Objective To investigate the effect of the treatment with prostaglandin El on neurogenesis after right middle cerebral artery occlusion in adult rats. Methods Thirty six rats were divided into the prostaglandin E1 （10ug·kg^-1·d^-1） group, vehicle group, and sham-operation group（n=l 2 each）, randondy.Rats were intraperitoneally injected with 5-bro- too-2 -deoxyuridine （BrdU） for labeling the cell proliferation. Half of the rats in each group were sacrificed at 7 and 14 d after stroke. Neurological behavior defects were examined before sacrifice. Hematein and Eosin（H ＆ E） stainings was used to examine cerebral infarction volume. Immunofluorescent staining was used to detect BrdU＋ cells in the ipsilateral peri-in- faretion area, BrdU＋ and BrdU＋/DCX＋ cells in the ipsilateral subventricular zone（SVZ） and the migration distance of BrdU＋/ DCX＋ cells from the ipsilateral SVZ to the cerebral infarct zone. Results Compared with the vehicle group or the sham-op- erated group, treatment with prostaglandin E1 significantly increased the number of BrdU＋ cells in the ipsilateral SVZ（7 d：380.3±14.3 vs. 251.3±9.5 vs. 50.3±5.4, 14 d： 230.2±10.1 vs. 126.2±8.8 vs. 24.3±6.3, all P〈 0.05） and in the ipsilateral peri-infarction area（7 d： 349.7±9.2 vs. 203.5± 12.2 vs. 53.8±8.4, 14 d： 203.4± 13.3 vs. 136.7±11.8 vs. 27.2±6.2, all P〈 0.05）. Compared with the vehicle group, treatment with prostaglandin E1 also significantly increased the number of BrdU＋/ DCX＋ cells in the ipsilateral SVZ （7 d： 209.0±19.6 vs. 109.8±14.4 vs. 27.3±5.9, 14 d： 96.2±13.0 vs. 47.3±6.8 vs. 25.7±6.2, all P〈 0.05）,augmented the migration distance of DCX＋/BrdU＋ from the ipsilateral SVZ to the cerebral infarct zone（7 d： 6039.3 ± 1035.6 μm vs. 3591.5 ± 716.6 μm, P〈0.05）, and improved neurological behavior（7 d： 1.5（1.0-2.0） vs. 2.0 （2.0-3.0）, 14 d： 0.5 （0-1.0） vs. 1.0（1.0-2.0）, P〈 0.05）. Conclusion The present results indicate that administr
出处
《中国神经精神疾病杂志》
CAS
CSCD
北大核心
2013年第6期326-330,共5页
Chinese Journal of Nervous and Mental Diseases
基金
国家自然科学基金资助青年项目(编号:81188098)
广东省自然科学基金资助项目(编号:9451022002003396)
关键词
脑梗死
前列腺素E1
神经再生
大鼠
Cerebral infarction Prostaglandin E1 Nerve regeneration Rats
