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袁国强,吴以岭,贾振华,吴正国,高怀林,吴相春,魏聪.通心络对大脑中动脉闭塞模型大鼠脑缺血后神经细胞凋亡的影响[J].中国中西医结合杂志,2007,(8):720-723
通心络对大脑中动脉闭塞模型大鼠脑缺血后神经细胞凋亡的影响
Experimental Study on Effect of Tongxinluo on Nerve Cell Apoptosis after Cerebral Ischemia in Middle Cerebral Arterial Obstructive Model Rats
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DOI:
中文关键词:  通心络胶囊  大脑中动脉闭塞  凋亡  Caspase-3  p53  热休克蛋白70
英文关键词:Tongxinluo Capsule  middle cerebral arterial obstruction  apoptosis  Caspase-3  p53  heat shock protein 70
基金项目:国家重点基础研究发展计划(973计划)资助项目(No.2005CB523301)
作者单位
袁国强 河北以岭医药研究院络病研究室 石家庄050035 
吴以岭 河北以岭医药研究院络病研究室 石家庄050035 
贾振华 河北以岭医药研究院络病研究室 石家庄050035 
吴正国 河北以岭医药研究院络病研究室 石家庄050035 
高怀林 河北以岭医药研究院络病研究室 石家庄050035 
吴相春 河北以岭医药研究院络病研究室 石家庄050035 
魏聪 河北以岭医药研究院络病研究室 石家庄050035 
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中文摘要:
      目的探讨通心络胶囊在缺血脑保护方面的作用机制。方法SD大鼠随机分为5组:假手术组、模型组、MK-801组、通心络大剂量组(简称TXLL)、通心络小剂量组(简称TXLS)。制备大鼠大脑中动脉闭塞(MCAO)模型后,MK-801组腹腔注射MK-8010.5mg/(kg.d),1次/天;TXLL、TXLS组分别给予1.0g/(kg.d)和0.5g/(kg.d)通心络原粉灌胃,2次/天。采用流式细胞、Western blot及RT-PCR技术,观察通心络对大鼠脑缺血后神经细胞凋亡、Caspase-3、p53和HSP70蛋白及mRNA表达的影响。结果通心络与MK-801均可明显降低模型大鼠缺血后各时间点脑部神经细胞凋亡百分率(P<0.05,P<0.01),以TXLL组效果最显著;模型组Caspase-3、p53蛋白及mRNA表达较假手术组明显增高,通心络和MK-801均可使其表达减低,TXLL组最显著(P<0.01);与模型组比较,各治疗组HSP70蛋白及mRNA表达明显增高(P<0.05,P<0.01)。结论通心络通过减少MCAO模型大鼠神经细胞凋亡率进而发挥脑保护作用,其机制可能与抑制细胞凋亡相关因子Caspase-3、p53表达、促进应激保护性HSP70表达有关。
英文摘要:
      Objective To explore the action mechanism of Tongxinluo Capsule (TXL) in protecting brain from ischemic damage. Methods SD rats were divided into five groups randomly, the sham operation group, the model group, the MK-801 group, the large and low dosage TXL groups (TXLL and TXLS). After the middle cerebral arterial obstructive (MCAO) model was established, peritoneal injection of MK-801 0.5 mg/kg per day was given to the MK-801 group, and 1.0 g/(kg·d) and 0.5 g/(kg·d) of TXL powder was administered in twice via gastrogavage to the two TXL groups respectively. The nerve cell apoptosis rate, protein and mRNA expressions of Caspase-3, p53 and heat shock protein (HSP70) were observed using flow cytometry, Western blot and RT-PCR technique. Results Both TXL and MK-801 could obviously lower the apoptosis rate in model rat (P<0.05,P<0.01), TXLL showed the optimal effect. Caspase-3, p53 protein and mRNA expression in the model group were obviously higher than those in the sham operated group. As compared with the model group, the expressions of Caspase-3 and p53 were lower and those of HSP70 and mRNA were higher in the two TXL and MK-801 groups (P<0.05 or P<0.01). Conclusion TXL displays it brain protective effect through reducing nerve cell apoptosis rate in MCAO model rats, the mechanism may be related to its actions in inhibiting apoptosis related factors Caspase-3 and p53, and promoting stress protecting factor HSP70.
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