目的　探讨热休克蛋白 - 70 (HSP70 )基因在缺氧缺血新生大鼠脑内的表达及地塞米松 (DEX)对其影响。方法　通过建立新生大鼠缺氧缺血性脑病动物模型 ,应用快速竞争性RT PCR技术 ,分别对缺氧缺血(HI) ,DEX预处理后予缺氧缺血 (DH) ,缺氧结束后即刻予DEX (HD) ,DEX加假手术 (DS) ,正常对照 (NS)五组动物的实验侧大脑组织中HSP70mRNA的表达进行半定量分析。结果　缺氧缺血后新生大鼠脑内HSP70mRNA的表达明显增强 ,其表达高峰 (3.86 8± 1.42 1)位于HI后 12h左右 ,并在 12～ 48h内维持较高水平 (3.186±0 .80 3,2 .5 6 8± 0 .70 9)。DEX预处理可使HSP70mRNA的表达明显下降或几乎完全被抑制 ,其 12h ,2 4h ,48h分别为 0 .5 2 6± 0 .5 93,0 .492± 0 .45 0 ,0 .434± 0 .42 8。HI后给予DEX对HSP70mRNA的表达则无明显影响。其12h ,2 4h ,48h分别为 3.46 0± 1.30 9,3.0 2 0± 0 .5 6 5 ,2 .2 42± 0 .5 0 4。结论　DEX预处理可抑制HI对HSP70mRNA过表达的诱导。推测DEX预处理后使HSP70mRNA的表达下降 ,可能与DEX抑制了神经元的过度兴奋有关。

Objective To investigate the expression of HSP70 gene in the brain of neonatal rats following cerebral hypoxia ischemia (HI) and the effect of dexamethasone (DEX) on the expression of HSP70 mRNA. Methods Rapid competitive reverse transcriptase PCR was used to semi quantitatively analyze the expression of HSP70 mRNA in the ipsilateral cerebral hemisphere in a neonatal rat model of hypoxia ischemia. Groups were divided into those pre treated with DEX prior to hypoxia ischemia, those treated with DEX immediately following hypoxia ischemia, those pre treated with DEX prior to sham, and normal controls, respectively. Results Cerebral HI increased HSP70 mRNA expression. The peak time of overexpression was 12 h after HI(3.868±1.421), and maintained at a higher level during 12～48 h(3.186±0.803, 2.568±0.709). The intensity of HSP70 mRNA expression was greatly decreased or almost abolished completely by the pretreatment with DEX. At 12 h, 24 h and 48 h after this treatment, HSP 70 mRNA expression were 0.526±0.593, 0.492±0.450 and 0.434±0.428, respectively, while the treatment with DEX after the insults had no evident effect on the expression of HSP70 mRNA. AT 12 h, 24 h and 48 h, HSP 70 mRNA expression were 3.460± 1.309 , 3.020±0.565 and 2.242±0.504, respectively. Conclusions DEX prophylaxis could suppress the overexpression of HSP70 mRNA following cerebral HI. Inhibition of HSP70 mRNA expression by DEX prophylaxis could be related to the suppression of overexcitation of neurons.