期刊文献+

热应激和短暂心肌缺血对大鼠心肝组织热休克蛋白70表达的影响 被引量:3

The effects of heat stress and brief myocardial ischemia on the expression of HSP 70 in heart and liver tissues of rats
下载PDF
导出
摘要 目的探讨热应激及短暂心肌缺血对大鼠心、肝组织损伤及热休克蛋白(HSP70)表达的影响。方法24只雄性SD大鼠随机分为:对照组、假手术组、热休克组和短暂心肌缺血组,每组6只,应激后20h取心、肝组织,采用Western blotting、免疫组化及HE染色方法,观察大鼠心、肝组织的病理变化和HSP70的表达。结果(1)热应激及短暂心肌缺血后大鼠心、肝组织均有病理改变且HSP70表达与对照相比均显著增加(P<0.05);(2)短暂心肌缺血后心肌中HSP70表达量显著高于热应激后的表达量(P<0.05),而肝脏在两种刺激后HSP70表达量差异无统计学意义(P>0.05)。结论短暂心肌缺血对心脏组织中HSP70表达的影响强于热应激,而对肝脏的影响两者无显著差异,这可能与不同刺激引起心、肝组织中HSP70表达机制不同有关。 [ Abstract] Objective To investigate the effects of heat stress and brief myocardial ischemia (BMI) on the pathological changes and expression of HSP 70 in heart and liver tissues of rats. Methods 24 male SD rats were randomly divided into 4 groups:control group,sham operation group,heat shock group and BMI group( n =6 in each group). The heart and liver tissues were taken 20h after heat shock and BMI to detect the expression of HSP70 by western blotting and immunohistochemistry. The pathological changes in heart and liver tissues of rats were observed by HE staining. Results ( 1 ) As compare with control group, there were significant pathological changes and increase of expression of HSP 70 in heart and liver tissues after BMI and heat shock ( P 〈 0.05 ). (2) The HSP70 expression of heart in BMI group was significanfly higher than that in heat shock group ( P 〈 0.05) ,while there was no significant difference in the expression of HSP70 of liver after the two stimulus ( P 〉 0.05). Conclusion The influence of BMI on HSP70 expression in heart is more obvious than that of heat stress, however, there is no significant difference in the influence on liver between the two stimulus, which may be related with the different mechanisms in expression of HSP70 of heart and liver after brief myocardial ischemia and heat shock.
出处 《河北医药》 CAS 2009年第17期2203-2205,共3页 Hebei Medical Journal
关键词 热休克蛋白70 热休克反应 心肌缺血 免疫组织化学 heat shock protein 70 heat shock reaction myocardial ischemia immunohistochemistry
  • 相关文献

参考文献6

二级参考文献54

共引文献48

同被引文献48

引证文献3

二级引证文献21

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部