摘要
目的:观察尿激酶型纤溶酶原激活物(uPA)及其抑制剂-1(PAI-1)在脑缺血再灌注大鼠缺血侧皮质区表达的变化和穴位埋药线及穴位注射干预对其的影响。方法:将SD大鼠随机分为正常组、假手术组、模型组、穴位注射组、穴位埋药线组。采用改良线栓法制备局灶性脑缺血再灌注模型。穴位埋药线组在"大椎""百会"穴埋入胶原川芎嗪缓释剂药线,穴位注射组在"大椎""百会"穴注射川芎嗪注射液。应用免疫组化法观察各组大鼠缺血皮质区中uPA、PAI-1表达。结果:模型组大鼠缺血区皮质区中uPA表达增高、PAI-1表达降低(P<0.01);与模型组相比,两治疗组均能下调uPA表达、上调PAI-1的表达(P<0.05,P<0.01),穴位埋药线的优势作用表现在3 d和5 d,与穴位注射组比较差异有统计学意义(P<0.05)。结论:穴位埋药线和穴位注射均可上调脑缺血再灌注大鼠缺血皮质区中PAI-1的表达,下调uPA表达,通过减轻脑微血管基底膜和内皮细胞的损害进而保护脑微血管结构的完整性;穴位埋药线的作用优于穴位注射。
Objective To observe the effect of acupoint-embedement of medicated-thread and acupoint-injection of Chuanxiongzine on the expression of urokinase-type plasminogen activator （uPA） and plasminogen activator inhibitor-1 （PAI-1） in the cerebral cortex in rats with cerebral ischemia-reperfusion injury （CI/RI）, so as to explore its underlying mechanism in protecting the ischemic cerebral tissue. Methods Seventy-eight SD rats were randomly divided into normal control group （n = 6）, sham operation （sham） group （n = 18）, model group （n = 18） ,acupoint injection （AI） group （ n = 18）, and acupoint-thread-embedment （ATE） group （n = 18）. Rats of the latter 4 groups were randomized into 1 d, 3 d and 5 d subgroups, with 6 rats in each. CI/RI model was established by occlusion of the right middle cerebral artery （MCAO） for 30 min and reperfusion. For rats of the AI group, Chuanxiongzine （0. 1 mL/200 g） was injected into ＂Baihui＂ （GV 20） and ＂Dazhui＂ （GV 14）, and for those of ATE group, a piece of medicated thread containing collagen protein （extracted from the rat＇s tail tissue） and Chuanxiongzine ＋ retarder was embedded into GV 20 and GV 14, respectively. The expression of uPA and PAI-1 in the cerebral cortex on the ischemia side was detected by immunohistochemistry. Results In comparison with the normal control group, the expression of uPA of the ischemia cerebral cortex on day 1, 3 and day 5 in the model group was increased significantly （P〈0.01）, while the PAI-1 expres sion decreased remarkably in the model group （P〈0, 01 ）. Compared with the 3 time-points of the model group, cortical uPA expression levels at the 3 time-points in the AI group and those of day 3 and day 5 in the ATE group were down-regulated significantly （P〈0.01）, whereas cortical PAI-1 expression levels at the 3 time-points in both AI and ATE groups up-regulated considerably （P〈0.05, P〈0.01）. Comparison between AI and ATE groups showed that the expression levels of cortical uPA in the latter group on day 3 and day 5 were significantly lower than those of the former group （P〈0.05）, whereas the cortical PAI-1 expression levels in the latter group on day 3 and day 5 were evidently higher than those of the former group （P〈0.05）. But, cortical PAI-1 expression of the ATE group on day 1 was significantly lower than that of the AI group （P〈0.05）. No significant differences were found between the AI and ATE groups in the expression level of cortical uPA on day 1 and between normal and sham groups in both uPA and PAI-1 expression levels at the 3 time-points （P〈0.05）. Conclusion Both AI and ATE can down-regulate cortical uPA expression and up-regulate cortical PAI-1 expression in rats with CI/RI, which may contribute to their protective effect in reducing cerebral ischemic injury.
出处
《针刺研究》
CAS
CSCD
北大核心
2010年第6期409-414,共6页
Acupuncture Research
基金
国家中医药管理局课题(0607JP27)
关键词
穴位埋药线
穴位注射
脑缺血再灌注
皮质区uPA和PAI-1表达
免疫组化
Acupoint-thread-embedment
Acupoint injection
Cerebral ischemia-reperfusion
Cerebral uPA and PAI-1 expression
Immunohistochemistry
