中文摘要：

目的：观察大鼠脑出血后内源性神经干细胞的激活、增殖状况。方法：采用大鼠尾状核注射自体动脉血建立脑出血模型，将大鼠分为假手术组、脑出血组、微创术干预脑出血组（微创组）3组，在3．0T磁共振下扫描观察血肿变化及鉴定建模成功，在第1、7、14、21天测评大鼠神经功能评分，检测Nestin与Brdu共表达的内源性神经干细胞激活和增殖及灶周小胶质细胞的活化情况。结果：MRI扫描发现微创术组于7～21d脑出血后灶周水肿减轻；第7、14天时免疫组化检测发现小胶质细胞激活受抑制，神经功能评分明显高于脑出血组和假手术组（均P〈0．01）；微创组内源性神经干细胞表达于7～21d呈逐渐增多的趋势，但与脑出血组及假手术组无统计学差异（P〉0．05）。结论：应用MRI仪器可成功观察大鼠微创血肿清除术和脑出血灶周水肿变化。微创术可减轻脑出血后灶周水肿、减轻神经功能缺损，其机制可能通过促进内源性神经干细胞激活增殖，抑制小胶质细胞活化，提高神经保护作用。

英文摘要：

Objective： To observe the activation and proliferation of endogenous neural stem cells （ENSCs） after mini- mally invasive evacuation of hematoma in rats with intracerebral hemorrhage. Methods ： The rat ICH models were established by injection of autologous blood into caudate nucleus. Rats were designed into sham operation group, intracerebral hemorrhage group and minimally invasive surgery group. The changes of hematoma were observed by 3.0 T MRI scan and the models were identified to be success. The neurological function score was evaluated. Nestin and BrdU expression of ENSCs activation and proliferation, the activation of perifocal microglial were detected at 1^th, 7^th, 14^th and 21 ^st day. Results： MRI scans showed that edema alleviated in minimally invasive surgery group 7 to 21 days after intracerebral hemorrhage. The activation of microglia cell was inhibited as showed by immunohistochemical detection in minimally invasive surgery group at Th, 14th day, and the neurological function score was significantly higher than that of intracerebral hemorrhage group and sham operation group （P 〈0. 01 ）. The expression of ENSCs showed a gradually increased trend at 7 to 21 days in minimally invasive surgery group, but there was no statistically significant difference compared with that of intracerebral hemorrhage group and sham operation group （P 〉 0.05 ）. Conclusions ： Minimally invasive evacuation of hematoma in rat model with ICH and changes of cerebral hemorrhage and edema can be observed successfully by MRI. Minimally invasive surgery reduces cerebral hemorrhage and edema as well as neurological deficits, which may be achieved by activation and proliferation of ENSCs, inhibition of the activation of microglia and enhancement of the neuroprotection.