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作 者:薛慎伍[1] 刘春寒[1] 张兆岩[1] 王娜[1]
机构地区:[1]济南军区总医院干部四科,山东济南250031
出 处:《实用医药杂志》2009年第5期43-45,49,共4页Practical Journal of Medicine & Pharmacy
摘 要:目的探讨依达拉奉在大鼠脑缺血性损伤中的作用及与TGF-β1、Bcl-2的关系。方法对72只大鼠用结扎离断法制作颈动脉局灶性慢性脑缺血模型。脑缺血3周腹腔注射依达拉奉3mg/kg为依达拉奉组(n=24),另设对照组(n=24)和脑蛋白水解组(n=24,3mg/kg腹腔注射脑蛋白水解物)。随后用卒中指数评分标准和神经病学症状评分标准评估大鼠神经功能损伤程度,用免疫组化病理切片染色观察脑组织中TGF-β1、Bcl-2的阳性表达细胞数。结果①脑缺血4周后,依达拉奉组大鼠的神经功能障碍明显轻于缺血对照组和脑蛋白水解物组;②脑缺血4周后依达拉奉组TGF-β1、Bcl-2阳性表达细胞均显著高于其它两组(P<0.01),而脑蛋白水解物组又高于缺血对照组(P<0.05);且在4~12周阳性细胞表达最高;③脑缺血后TGF-β1、Bcl-2阳性表达细胞在额叶皮层最明显,海马次之。结论依达拉奉对大鼠脑缺血性损伤的保护作用,其机制可能是通过上调TGF-β1、Bcl-2水平,清除自由基,降低羟自由基浓度,抑制脂质过氧化。Objective To investigate the contribution of Edaravone on chronic cerebral ischemia and expression of TGF-β1 and Bcl-2 in rats. Method Chronic cerebral ischemic model was established by ligation of bilateral carotid artery in rats. Edaravone was peritoneally injected at 3mg/kg later 3 weeks after operation. The neural function impairment was evaluated by Stroke Index and Neurological Symptom Score. The positive expression of TGF-β1 and Bel-2 was detected by pathological section and immunohistochemistry stain. Result ①The neurological disfunction in Edaravone group was significantly gentle than that of control group and Cerebrolysin Vial group later 4 weeks after cerebral ischemia;②The positive expression of TGF-β1 and Bcl-2 was significantly higher than that of the other two groups 4 weeks after operation(P〈0.01). The positive expression in Cerebrolysin Vial group was higher than that of control group (P〈0.01). The positive expression was highest during 4 to 12 weeks; ③The most obviously expression of TGF-β1 and Bcl-2 was in frontal lobe, that in hippocampus was secondary. Conclusion Edaravone can protect neural tissue against ischemic injury in rats.The mechanism includes up-regulation of the expression of TGF-β1 and Bcl-2, elimination of free radical, depression of the concentration of hydroxy radical and inhibition of lipid peroxidation.
分 类 号:R743-33[医药卫生—神经病学与精神病学]
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