热休克蛋白70对大鼠脑干损伤诊断的免疫组织化学研究

Immunohistochemical research on brain stem injury：expression of heat shock protein 70 in rat brain after traumatic brain stem injury

为了解脑干在受到创伤后作为降解异常蛋白的分子伴侣（molecularchaperones）之一的热休克蛋白70（heatshockprotein70HSP70）在中枢神经系统的表达情况，用免疫组化法对Wistar大鼠脑干针刺损伤模型的HSP70在损伤前及损伤后1、3、6、12、24小时的中枢神经各区的表达数量、分布变化进行检测。在针刺后1小时脑组织HE染色尚无明显特异性改变的情况下，大脑及小脑内HSP7免疫活性阳性的血管内皮细胞、神经胶质细胞显著增加，在损伤灶局部周围出现HSP7I免疫活性阳性神经元细胞增多，伤后3小时该处HSP7阳性神经元数量显著多于伤前及同一时间点的其它处脑组织，伤后24小时HSP7阳性细胞依然广泛存在。脑干的外伤性损伤可导致脑组织的蛋白质结构发生改变，脑干局部HSP70阳性神经元数量增多可作为脑干损伤定位诊断的依据。

The aim of this study was to determine the expres-sion of heat shock protein 70 （HSP70）as molecular chap-erones ，following tratunatic brain stem injury （TBSI） Theexpression HSP70 was detected in respective brain re-gions of rats 1h, 3h, 6h, 12h, 24h after brain stem stab-bing wound. Numerous HSP70 immunoreactivity positive blood vessel endothelioid and glia cells were found in ce-rebral, cerebellar cortex and hippocampus after lh, withH. E stain unchanged. In the area near the focal of brainstem injury ，HSP70 immunoreactivity positive neurons in-creased significantly after 1h of injury, reaching the high-est level ds 3h, much higher than in other areas.HSP70 immunoreactivity positive cells still existed after24h of injury. It was suggested that TBSI cause the de-fectiveness of protein structure in brain， and induceHSP70 proteolysis of denature Protein including mistold-ing or aggregate. TBSI can be diagnosed regionally by theincreasing of HSP70 immunoreactivity positive neurons in the focal of brain stems.