摘要
目的:观察银杏叶提取物预处理对小鼠脑缺血损害的影响和CD11b阳性细胞反应变化。方法:实验于2005-03/06在大连医科大学脑疾病研究所进行。采用随机对照的方法将120只Balb/c小鼠随机分成6组:空白对照组、单纯照射30min组、注射玫瑰红组、缺血组、银杏叶提取物预处理组、地塞米松处理组,每组20只。将银杏叶提取物100mg/(kg·d)腹腔注射预处理7d后,以光化学法建立局灶性小鼠脑缺血模型;运动捕捉系统分析局灶性脑缺血模型小鼠行为学变化;在相应时间点(分别为3h,1,3,7d)处死动物(每个时间点5只),红四氮唑染色观察脑梗死体积;尼氏染色观察组织学变化,CD11b免疫组织化学染色检测小胶质细胞反应。结果:无补充鼠参加实验,120只小鼠均进入结果分析。①与对照组相比,脑缺血组缺血后1d小鼠左右侧上、下肢肢体抬高高度的差值高[(0.2921±0.0674),(0.1740±0.053)cm,P<0.001,P<0.01],银杏叶提取物预处理和地塞米松处理可逆转这一变化。②局灶性脑梗死缺血后24h,与缺血组相比,银杏叶提取物预处理组和地塞米松处理组损害皮质的脑缺血梗死体积明显减少[(9.89±1.01),(7.23±1.45),(6.99±1.21)mm3,P<0.01]。③尼氏染色显示缺血周边皮质神经元数量显著增多(P<0.01)。④脑缺血后1d,3d,7d皮质缺血周边区CD11b-IR阳性细胞数减少(P<0.001),平均灰度增加(P<0.001)。银杏叶提取物预处理组和地塞米松处理组之间差异均无显著性。结论:银杏叶提取物预处理可能通过降低小胶质细胞反应而产生对小鼠脑缺血明显的神经保护作用。
AIM： To observe the neuroprotective effects of Ginkgo biloba extract （GBE） on mice focal cerebral ischemia and the responses of CD11b-immunoreactivity （CD 11 b-IR） positive cell.
METHODS： The experiment was conducted in the Institutes for Brain Disorder, Dalian Medical University from March to June 2005. With the randomized controlled method, 120 Balb/e mice were divided into six groups： control group, illumination for 30 minutes group, rose begnal group, ischemia group, GBE pretreatment group, and Dexamethasone （DEX） treatment group with 20 mice in each group. GBE was pretreated with intrapcritoneal doses of 100 mg/kg per day for 7 days to establish mice models of focal cerebral ischemia with photochemistry method. Movement Capture Analysis was used to evaluate the motion ability of mice models; the animals were killed （5 mice at each time point） at different time points （3 hours, 1, 3, and 7 days）, and 2, 3, 5-triphenyhetrazolium chloride was used to observe the infarction volume; Nissl staining was adopted to observe the histological changes, and microglia response was assessed by immunohistochemistry of CD11b.
RESULTS： All the 120 mice were involved in the result analysis without supplement. ①Compared with the control group, the average height in bilateral forelimbs and hindlimbs after isehemia for 1 day of the ischemia group was higher [（0.292 1±0.067 4）, （0.174 0±0.05 3） cm, P 〈 0.001, P 〈 0.01], and GBE pretrcatment and DEX treatment could significantly decrease the difference, ②After 24 hours of focal infarction ischemia, compared with the ischemia group, a significant reduction of infarction volume was found in the GBE pretreatment group and DEX group [（9.89±1.01）, （7.23±1.45）, （6.99±1.21） mm^3, P 〈 0.01]. ③Nissl staining revealed that the number of neurons was increased in the lesion periphery of ischemia （P 〈 0.01）.④The number of positive CD11b-IR significantly reduced （P 〈 0.001） and the main gray （P 〈 0.001） of CD11b-IR in the lesion periphery of ischemia was increased after ischemia 1, 3 and 7 days. There was no significant difference in every index between GBE pretreatment group and DEX treatment group.
CONCLUSION： GBE exerts neuroprotection after focal cerebral ischemia through inhibiting the response of microglia in brain.
出处
《中国临床康复》
CSCD
北大核心
2006年第43期55-57,共3页
Chinese Journal of Clinical Rehabilitation
基金
国家自然科学基金(30470682)
辽宁省重点实验室专项资金(37)
辽宁省优秀青年科研人才培养资金(3050006)~~
