摘要
目的探讨丁苯酞注射液在大鼠脑缺血再灌注损伤中的神经保护作用及可能的作用机制。方法56只清洁级SD大鼠,随机平均分为假手术组,缺血—再灌注组,丁苯酞24 h治疗组,丁苯酞48 h治疗组。缺血2 h再灌注时,丁苯酞24 h治疗组及丁苯酞48 h治疗组分别予腹腔注射丁苯酞注射液每天20 mg/kg,直至各时间点处死。假手术组和缺血—再灌注组分别向腹腔注射等量生理盐水。观察各组脑缺血体积及脑源性神经营养因子(BDNF)阳性细胞数。结果丁苯酞治疗组比缺血再灌注组的脑缺血体积明显缩小,且丁苯酞48 h治疗组较24h治疗组缩小更显著(P<0.05)。BDNF阳性细胞检测显示丁苯酞治疗组比缺血再灌注组的BDNF阳性细胞数明显增加,且丁苯酞48 h治疗组较24 h治疗组增多更明显,差异均具有统计学意义(P<0.05)。结论丁苯酞注射液可能通过诱导BDNF的表达从而发挥对大鼠脑缺血再灌注损伤的神经保护作用。
Objective To investigate the neuroprotection of Butylphthalide in mice after ischemia-reperfusion injury and its mechanism. Methods 56 clean-healthy SD rats were randomly divided into four groups：sham group, ischemic- reperfusion group, NBP for 24 hours group, NBP for 48 hours group.At the time of reperfusion after ischemia 2 h, the two NBP groups were treated with NBP （20 mg/kg, QD） by intraperitoneal injection until they were executed, also the sham group and the ischemic-reperfusion group were treated with the same dose of normal saline by intraperitoneal injection. Results The volume of cerebral ischemia in NBP-greup was smaller than the ischemic-reperfusion group,what was more, the NBP-48 group was much more smaller than NBP-24 group, all had statistical significance（P〈0.05） .The number of BD- NF-positive cell in NBP-group was much more than the ischemic-reperfusion group, and NBP 48-greup increased more obviously than NBP-24 group,the difference was statistically significant （P〈0.05）. Conclusion Butyl phthalide injection can induce the expression of BDNF and have protective effect on rats nerve with ischemia-repeffusion injury.
出处
《中南医学科学杂志》
CAS
2016年第3期275-278,282,共5页
Medical Science Journal of Central South China
关键词
丁苯酞
SD大鼠
脑缺血
再灌注损伤
脑源性神经营养因
Butylphthalide
SPrague,Dawley rats
brain ischemia
reperfusion injury
brain derived neurotrophic factor
