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热休克蛋白70抑制大鼠颅脑损伤诱生型一氧化氮合酶mRNA的表达
引用本文:毛定安,杨于嘉,虞佩兰,尹飞,黄榕. 热休克蛋白70抑制大鼠颅脑损伤诱生型一氧化氮合酶mRNA的表达[J]. 中华实验外科杂志, 2001, 18(1): 64-66
作者姓名:毛定安  杨于嘉  虞佩兰  尹飞  黄榕
作者单位:湖南医科大学湘雅医院儿科
基金项目:国家自然科学基金资助项目(39870251)
摘    要:
目的 探讨热休克蛋白70(HSP70)对大鼠感染性脑损伤(感脑)诱生型一氧化氮合酶(iNOS)的表达及一氧化氮(NO)合成的影响。方法 将大鼠72只随机分为正常对照组、感染性脑损伤组和热休克处理组,每组又h共3个时间点。采用百日咳菌液通过左颈内动脉注入制成大鼠感染性脑损伤模型,用Western印迹杂交技术检测各组各时间点的HSP70的表达,同时用原位杂交方法检测各组iNOSmRNA的表达及Griess法测定各组的NO含量的变化。结果 Western印迹杂交分析结果表明,大鼠感脑各组及正常组有一定量的HSP70表达,而热休克处理组的HSP70的量明显高于感脑组(P〈0.01)。原位杂交结果提示iNOS在感脑的大脑皮质神经细胞4、8、24h开始表达,可见明显的杂交信号,而休克处理组仅有少量的阳性颗粒。NO含量在感脑

关 键 词:颅脑损伤 热休克蛋白70 一氧化氮合酶 大鼠 mRNA
修稿时间:2000-02-16

Heat shock protein 70 inhibited inducible nitric oxide synthase gene expression in infectious cerebral injury in rat
MAO Dingan,YANG Yujia,YU Peilan,et al.. Heat shock protein 70 inhibited inducible nitric oxide synthase gene expression in infectious cerebral injury in rat[J]. Chinese Journal of Experimental Surgery, 2001, 18(1): 64-66
Authors:MAO Dingan  YANG Yujia  YU Peilan  et al.
Affiliation:MAO Dingan,YANG Yujia,YU Peilan,et al.Department of Pediatrics,Xiangya Hospital,Hunan Medical University,Changsha 410008,China [
Abstract:
Objective To study the effects of heat shock protein 70 (HSP70) on inducible nitric oxide synthase (iNOS) expression and nitric oxide (NO) synthesis in infectious cerebral injury in rat. Methods The infectious cerebral injury model was developed by injection of Pertussis Bacilli (PB) suspension via the left internal carotid artery. A total of 72 rats were divided randomly into 3 groups: normal saline control group (NS group), infection cerebral injury group (PB group) and HSP70 pretreatment group (HSP group). The animals were decapitated at 4 h, 8 h and 24 h after injection of PB or NS. HSP70 expression in brain tissue was detected by using Western blot analysis. iNOS mRNA expression in brain tissue was determined by using in situ hybridization method and NO in the brain homogenate was determined by using Griess method. Results Western blot analysis showed HSP70 in brain tissue elevated after heat shock response (HSR), whereas the level of HSP70 in the HSP group was significantly higher than in the PB group ( P <0.01). The signals of iNOS mRNA expression were observed in NS group, PB group and HSP group at 4th h. Hybridization signals in the PB group were significantly stronger than those in the HSP group at 8th h and 24th h. Similarly, the concentration of NO in the PB group was significantly increased, while decreased in the HSP group ( P <0.01). Conclusion The HSR might inhibit iNOS mRNA expression and the increase of NO, which might be associated with the induction of HSP70 synthesis in brain tissue, suggesting that HSP70 may be protective against infectious cerebral injury. [
Keywords:Cerebral injury  Heat shock proteins  Nitric oxide synthase  Rat
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