摘要
目的:观察生脉注射液对小鼠局灶性脑缺血再灌注损伤后的神经保护作用及组织因子(TF)表达及相关信号通路的影响。方法:C57BL/6J小鼠随机分成假手术组、缺血再灌注组、生脉注射液高、中、低剂量组(5.68,2.84,1.42 g.kg-1)。采用线栓法复制小鼠大脑中动脉栓塞模型,缺血1 h后ip不同剂量生脉注射液,再灌注24 h后观察小鼠脑梗死面积、神经行为学评分等指标。同时采用蛋白印迹技术测定缺血1 h,再灌注1 h后脑组织中TF,核转录因子κB(NF-κB/p65),蛋白激酶B(Akt)等蛋白的表达与磷酸化情况。结果:与模型组相比,高、中剂量生脉注射液可显著降低脑缺血再灌注小鼠的脑梗死率,提高神经行为学评分,并呈现一定的剂量依赖性。生脉注射液可显著下调缺血再灌注1 h诱导的模型小鼠脑组织TF的表达,同时抑制NF-κB的激活与Akt的磷酸化。结论:生脉注射液在一定剂量范围内,可显著改善小鼠脑缺血再灌注损伤,其作用机制可能与抑制TF的异常表达及相关的NF-κB和Akt通路活化有关。
Objective： To investigate the neuroprotective effect of Shengmai injection （SMI） on the expression of tissue factor （TF） and related signal pathways in mice with cerebral ischemia-reperfusion injury. Method： Mice were randomly divided into 5 groups as following： sham operation group, ischemia-reperfusion （I/R） group, SMI groups at three doses （5.68, 2.84, 1.42 g .kg-1 ）. Right middle cerebral artery was occluded by inserting a thread through internal carotid artery for 1 h. The infarct volume and neurological scores were evaluated after 24 h reperfusion. Western blotting was used to determine the expression of tissue factor （TF） , nuclear factor-kappa B （NF-KB） subunit p65, Akt, and their phosphorylation after 1 h reperfusion. Result： Compared with I/R group, SMI could significantly reduce the infarct volume and improve the neurological deficits in a dose-dependent manner. SMI also remarkably down-regulated the expression of TF, inhibited the activation of NF-KB induced by ischemia-reperfusion and the phosphorylation of Akt in mice. Conclusion： Shengmai injection, at certain dosage range, elicits potent protection against cerebral ischemia/reperfusion injury, which may partly be due to inhibiting TF expression and its related pathways.
出处
《中国实验方剂学杂志》
CAS
北大核心
2013年第14期194-199,共6页
Chinese Journal of Experimental Traditional Medical Formulae
基金
国家自然科学基金项目(81274004)
天然药物活性组分与药效国家重点实验室自主科研重点项目(JKGZ201107)
2011江苏高等学校优秀科技创新团队项目
江苏省优势学科建设项目
江苏省研究生创新计划(CXZZ11-0797)
