摘要
目的通过观察缺血-再灌注损伤大鼠脑梗死的面积及神经学缺陷的程度,了解川芎嗪对大鼠脑缺血-再灌注的影响,探讨其有效剂量和量效关系;用免疫组织化学检测观察脑梗死组织ED1、IL-1β和TNF-α之表达,探讨川芎嗪的作用机制。方法应用改良线栓法复制缺血-再灌注脑梗死动物模型。将健康成年66只SD雄性大鼠随机分为11组,实验结束后处死大鼠,将假手术组Ⅰ组、模型对照组Ⅰ组、TMP治疗组(Pre-100)Ⅰ组、治疗组(Pre-120)、治疗组(Pre-140)及MK801组Ⅰ组中的脑组织切取材制片、TTC染色、福尔马林固定后,采用病理图像分析系统,评价TMP是否能减少脑梗死面积;将假手术组Ⅱ组、模型对照组(Control)Ⅱ组、治疗组(Pre-100)Ⅱ组和MK801组Ⅱ组中大鼠的脑组织取材制片后,用免疫组织化学染色,观察ED1、IL-1β和TNF-α的阳性表达。结果(1)缺血前川芎嗪各剂量治疗组及缺血后30min川芎嗪治疗组均可减少缺血90min、再灌流24h脑梗死面积的形成并改善神经学缺陷。(2)缺血前治疗组川芎嗪100mg/kg同时也可以减少脑梗死区域内的ED1、IL-1β和TNF-α之免疫阳性表达。结论(1)川芎嗪可以减少大鼠缺血-再灌注脑梗死的形成并改善其神经学缺陷;(2)川芎嗪的治疗效用可能与抑制小胶质细胞活化、IL-1β和TNF-α的免疫阳性表达有关,并且推论川芎嗪可以用于治疗人脑梗死病。
Objective The first aim is to find out Tetramethyl Pyrazine＇s （TMP） effect for trea ting cerebral infarct and to research the effective dose and the relation between dose and effect, by observing infarction areas and neurological severity scale of rats＇ cerebral infarct caused by cerebral ischemia -reperfusion; and the second aim is to research TMP＇s function mechanism by observing the changes of the expressions of ED1, TNF-α and IL-1β in the immuno- reacting cells in the infarction region by using immunohistochemistry assay. Methods The cerebral infarct animal model was reproduced by use of modified thread- tie method. Sixty- six SD male adult rats in healthy condition were randomly and averagely divided into eleven groups. Take all the rats of Sham Group l, Control Group 1, TMP- treatment （Pre-100） Group 1, Treatment （Pre-120） Group, Treatment （Pre-140） Group, and MK801 Group 1 to evaluate whether TMP can decrease the ratio of cerebral infarction area, by analyzing the TTC-stained and formalin fixed brain tissue slices that were originally taken from the above-mentioned killed rats, with Pathology Image Analysis System. Also observe the positive expressions of ED1, IL-1β and TNF-α in the immuno-reacting cells in cerebral infarction brain tissue slice taken from the killed rats of Sham Group2, Control Group 2, Treatment （Pre- 100） Group 2, and MK801 Group 2. Results （1）The founding indicates that all the pre-treatment groups and post treatment group （30 minutes） using TMP can decrease the ratio of cerebral infarction area and improve the neurological deficit after 90 minute-ischemia and 24- hour- reperfusion. （2） Pre- treatment of TMP 100 mg/kg also decreases the immuno- positive expressions of ED1, TNF-α and IL- 1β in the cerebral infraction area. Conclusions （1） TMP can decrease the formation of cerebral infarction caused by cerebral ischemia-reperfusion and improve neurological deficits, and （2） TMP may be used to treat cerebral infarct in human, and its eff
出处
《神经疾病与精神卫生》
2008年第6期438-442,共5页
Journal of Neuroscience and Mental Health
关键词
川芎嗪
脑梗死
神经学缺陷
缺血-再灌注脑损伤
Tetramethyl pyrazine
Cerebral infarction
Neurological deficit
Cerebral ische- mia- reperfusion injury
