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机构地区:[1]桂林三金药业股份有限公司,广西桂林市541004 [2]中南大学药学院药理系,湖南省长沙市410078
出 处:《国际神经病学神经外科学杂志》2009年第4期303-306,共4页Journal of International Neurology and Neurosurgery
摘 要:目的研究脑脉泰对大鼠脑缺血再灌注损伤神经细胞凋亡和Akt、bcl-2、Bax、caspase3表达的影响。方法采用大鼠大脑中动脉栓塞再灌注动物模型,将雄性SD大鼠随机分为假手术组(sham)、脑缺血再灌注模型组(MCAO)、脑脉泰大剂量组(MCAO+脑脉泰2.24g/kg)、脑脉泰中剂量组(MCAO+脑脉泰1.12g/kg)、脑脉泰小剂量组(MCAO+脑脉泰0.56g/kg),每组10只大鼠。脑脉泰组在MCAO前5天开始灌胃给药,连续5d。用TUNEL法和免疫组化染色法分别检测缺血半暗带凋亡细胞和Akt、bcl-2、Bax和caspase3表达。结果脑脉泰大剂量组和中剂量组大鼠脑缺血半暗带的凋亡细胞显著减少(P<0.01),Akt、bcl-2表达显著增加,caspase3和Bax表达减少,与MCAO模型组比较,有显著性差异(分别为P<0.05和P<0.01)。结论脑脉泰对脑缺血/再灌注损伤有保护作用,其保护作用与促进Akt和bcl-2的表达,抑制Bax和caspasse3的表达有关。Objective To investigate the effects of Naomaitai on neuron apoptosis and the expression of Akt, bcl-2, Bax and caspase3 in rats with local cerebral ischemic reperfusion. Methods Male Sprague-Dawley rats were randomized into five groups ( n = 10 each) : sham-operated, middle cerebral artery occlusion (MCAO), Naomaitai treatment MCAO (2.24, 1.12 and 0.56 g/kg). Focal cerebral ischemia/reperfusion model was prepaved by transient occlusion of the middle cerebral artery for 90 minutes followed by 24 hrs reperfusion. Naomaitai was administered daily five days before operation. Twenty-four hrs after reperfusion, the brains were obtained for TUNEL staining, and Akt, bcl-2, Bax and caspase3 expression was detected by immunohistochemistry method. Results In the 1.12 g/kg and the 2.24 g/kg Naomaitai treatment groups, the apoptotic cells significantly decreased compared with the MCAO group (P 〈 0.01 ). The protein expression of Bax and caspase3 was lower, while the Akt and bcl-2 protein expression were significantly higher in the Naomaitai treatment groups (1.12 g/kg and 2.24 g/kg) than those in the MCAO group (P 〈0.05, P 〈0. 01 ). Conclusions Naomaitai may have protective effects against cerebral ischemic reperfusion injury, possibly through increasing expression of Akt and bcl-2, and decreasing expression of Bax and caspase3.
关 键 词:脑脉泰 脑缺血 细胞凋亡 AKT bcl-2 BAX CASPASE3
分 类 号:R741[医药卫生—神经病学与精神病学]
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