Exogenous kallikrein enhances neurogenesis and angiogenesis in the subventricular zone and the peri-infarction region and improves neurological function after focal cortical infarction in hypertensive rats
Exogenous kallikrein enhances neurogenesis and angiogenesis in the subventricular zone and the peri-infarction region and improves neurological function after focal cortical infarction in hypertensive rats
复制标题
外源性激肽释放酶增强高血压大鼠脑室下区和梗死周围区域的神经发生和血管生成，改善局灶性皮质梗死后的神经功能
DOI：
10.1016/j.brainres.2008.01.099
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发表时间：
2008-04-24
期刊：
影响因子：
2.9
通讯作者：
Zeng, Jinsheng
中科院分区：
文献类型：
--
作者：
Ling, Li;Hou, Qinghua;Zeng, Jinsheng
激肽释放酶（Kallikrein）是一种丝氨酸蛋白酶，最近被鉴定为血管生成生长因子。我们研究了外源性激肽释放酶延迟治疗是否能增强易发生中风的肾血管性高血压大鼠局灶性皮质梗死后的神经发生和血管生成。从远端大脑中动脉闭塞（MCAO）后24小时开始，连续6天每天通过尾静脉给予人组织激肽释放酶（1.6 x 10(-2) PNAU/kg）或载体。使用 5'-溴-2'-脱氧尿苷（BrdU，50 mg/kg）检查细胞增殖。分别在MCAO后3、7、14或28天处死大鼠。与媒介物组相比，在 MCAO 后 3 天开始，用激肽释放酶治疗显着增加了室下区 (SVZ) 和梗死周围区域中的 BrdU(+) 细胞数量（所有 p
Kallikrein, a serine proteinase, has been identified as an angiogenic growth factor recently. We investigated whether delayed treatment with exogenous kallikrein enhances neurogenesis and angiogenesis after focal cortical infarction in stroke-prone renovascular hypertensive rats. Human tissue kallikrein (1.6 x 10(-2) PNAU/kg) or vehicle was given through a tail vein daily for 6 consecutive days starting 24 h after distal middle cerebral artery occlusion (MCAO). Cell proliferation was examined by using 5'-bromo-2'-deoxyuridine (BrdU, 50 mg/kg). Rats were sacrificed at 3, 7, 14 or 28 d after MCAO, respectively. Treatment with kallikrein significantly increased the number of BrdU(+) cells in the subventricular zone (SVZ) and the peri-infarction region initiating 3 d after MCAO compared with the vehicle group (all p