摘要
目的:研究刺五加注射液对大鼠脑缺血损伤的保护机制。方法:Wistar大鼠随机分为假手术组、脑缺血模型组和刺五加注射液组(45、90mg/kg),腹腔注射给药,连续7d。末次给药后30min,采用大鼠大脑中动脉内栓线阻断法制备局灶性脑缺血损伤24h模型,通过硫代巴比妥酸法、化学比色法、TUNEL及免疫组化等方法,观察刺五加注射液对脑缺血损伤大鼠脑组织丙二醛(MDA)含量和超氧化物歧化酶(SOD)活性、大脑皮质区细胞调亡及bcl-2、bax和caspase-3基因蛋白表达的影响。结果:刺五加注射液(45、90mg/kg)可明显降低MDA含量,提高SOD活性,抑制神经细胞调亡,增加bcl-2蛋白表达,减少bax和caspase-3蛋白表达。结论:刺五加注射液对脑缺血损伤的保护机制可能与抗自由基、抑制细胞调亡有关。
AIM：To investigate the protective mechanism of acanthopanax senticosus injection（ASI） on focal cerebral ischemia injury in rats.METHODS：Wistar rats were randomly divided into sham operated group,model control group and two ASI groups,to which ASI of 45 and 90 mg/kg was intraperitoneally administered for 7d,and then subjected to cerebral ischemia injury induced by middle cerebral artery occlusion（MCAO） in rats,via string ligation of arteria carotis interna.The content of maleic dialdehyde（MDA） was determined by thibabituric acid（TBA） test and the activity of superoxide dismutase（SOD） was detected by chemical colorimetry test in cerebral tissues.Apoptosis in cortex region was measured with TUNEL method.Bcl-2,bax and caspase-3 protein expression of neurons was detected with immunohistochemistry staining in cortex region.RESULTS：ASI（45,90 mg/kg） could significantly decrease the content of MDA and increase the activity of SOD,and inhibit the neuronal apoptosis.ASI（45,90 mg/kg） could increase the expression of bcl-2 protein,and reduce the expression of bax and caspase-3 protein significantly.CONCLUSION：The protective mechanism of ASI on focal cerebral ischemia injury may be related to anti-free radical effect and inhibition of neuron apoptosis.
出处
《中国临床药理学与治疗学》
CAS
CSCD
2007年第9期1032-1036,共5页
Chinese Journal of Clinical Pharmacology and Therapeutics
关键词
刺五加注射液
脑缺血
自由基
细胞凋亡
acanthopanax senticosus injection
cerebral ischemia
free radical
apoptosis
