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贾瑞喆,蒋犁,乔立兴.黄芪对新生鼠缺氧缺血脑损伤后皮质的治疗作用[J].中国中西医结合杂志,2005,(1):54-57
黄芪对新生鼠缺氧缺血脑损伤后皮质的治疗作用
Study on Effect of Radix Astragali on Injury of Cerebral Cortex in Neonatal Rats after Hypoxia/Ischemia Brain Damage
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DOI:
中文关键词:  脑缺氧  脑缺血  半胱氨酸蛋白酶  凋亡  黄芪
英文关键词:cerebral hypoxia  cerebral ischemia  cysteinyl aspartate proteinase  apoptosis  Radix Astragali
基金项目:江苏省科委社会发展基金资助项目 (No .BS - 980 58)
作者单位
贾瑞喆 东南大学临床医学院 南京210009 
蒋犁 东南大学临床医学院 南京210009 
乔立兴 东南大学临床医学院 南京210009 
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中文摘要:
      目的探讨新生儿围产期缺氧缺血脑损伤 (hypoxia ischemiabraindamage ,HIBD)时皮质区神经细胞损伤的机制和黄芪对皮质区的神经保护作用。方法建立新生大鼠HIBD模型 ,分假手术组 (Sham组 )、模型组、黄芪治疗组。于缺氧后不同时间点取脑 ,分别行组织病理学检查并计数皮质区神经细胞死亡率、免疫组化检测结扎侧皮质区半胱氨酸蛋白酶 3(caspase 3)蛋白的表达、半定量逆转录 -聚合酶反应 (RT PCR)检测caspase 3mRNA表达。结果模型组结扎侧皮质caspase 3mRNA和蛋白表达于缺氧缺血 (HI)后 6h轻度升高 ,2 4h达高峰 ,4 8h后下降 ,5天和 7天时恢复至基础水平。黄芪治疗组HI后结扎侧皮质神经细胞死亡率明显降低、caspase 3mRNA和蛋白的表达峰值降低了 4 5 % (mRNA)、4 0 %~ 4 3% (蛋白 )。结论黄芪对未成熟脑HIBD后皮质部位有明显的神经保护功能 ,此功能与抑制caspase 3的表达有关。
英文摘要:
      Objective To study the mechanism of injury of cortical nerve cell in the newborn with hypoxia/ischemia brain damage (HIBD), and the neuroprotective effect of Radix Astragali (RA). Methods Neonatal HIBD model rats were established and divided into the sham group, the model group and the RA group. Brain of rats obtained at different time points after HIBD to conduct histopathological examination, neuron death rate count, as well as determination of caspase 3 (cysteinyl aspartate specific proteinase 3) protein mRNA expression in cerebral cortex by immunohistochemistry, semi quantitative reverse transcription polymerase chain reaction (RT PCR) respectively. Results In the model group, caspase 3 mRNA and protein showed an increase at 6 hrs, reached the peak at 24 hrs, and decreased at 48 hrs after HIBD, on the 5th and 7th day restored to baseline level. After being treated by RA, the neuron death rate of ligated side was obviously reduced, caspase 3 mRNA and protein expression peak value decreased by 45% (mRNA) and 40%-43% (protein). Conclusion RA shows markedly neuron protection in immature brain cortex after HIBD, which is related with the inhibition on caspase 3 expression.
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