脑干热休克蛋白70的表达与实验性脑损伤猝死的相关性

目的了解脑损伤后热休克蛋白 ７０（Ｈｅａｔ－ｓｈｏｃｋ ｐｒｏｔｅｉｎ ７０， ＨＳＰ７０）蛋白质及 ｍＲＮＡ在脑干局部的改变，及其对维持 脑干生命中枢功能的作用。方法用头颅打击器制成大鼠脑损伤猝死模型，免疫组化法分别测定损伤组损伤前和损伤 后 １、３、６、１２ ｈ及损伤摔死组脑于 ＨＳＰ７０的数量和分布变化；逆转录多聚酶链反应（ＲＴ－ＰＣＲ）检测各组相应部位 ＨＳＰ７０ ｍＲＮＡ水平。结果在脑损伤 １５ ｍｉｎ后脑干 ＨＳＰ７０ｍＲＮＡ水平显著升高， ＨＳＰ７０蛋白质需 ３～６ ｈ才大量表达；损伤后 猝死的鼠脑中仅见 ＨＳＰ７０ ｍＲＮＡ升高，ＨＳＰ７０蛋白质与对照组无差异。结论脑损伤后 ＨＳＰ７０合成迅速增加，清除损伤 因素，维持自稳状态；当损伤严重时，应激蛋白质的合成障碍，抗损伤的保护机制不能发挥，脑干生命中枢的功能紊 乱，生命丧失。因此， ＨＳＰ７０ ｍＲＮＡ－蛋白质分离可作为神经细胞致死性损伤的标志。

Correlation between expression of heat-shock protein 70 in the brain stem and sudden death after traumatic brain injury:an experimental study

Objective To investigate the patterns of heat-shock protein 70 (HSP70) biosynthesis following traumatic brain injury and observe its effect on the function of the brain stem. Methods Animal models of traumatic brain injury were established in rats using self-designed devices, and the expression of HSP70 in the brain stem 1,3,6,12 h after the injury in injury group and immediately after death in sudden death group respectively,was determined immunohistochemically. HSP70 mRNA was measured by RT-PCR 15,30 min and 1,3,6 h after injury and following sudden death respectively. Results In the injury group, the level of HSP70 mRNA in the brain stem was evidently elevated as early as 15 min following impact-in- duced brain injury,while profuse expression of HSP70 was observed till 3 to 6 h after the injury.The levels of HSP70 mRNA, but not the protein itself, were elevated in the brain stem of the rats in sudden death group. Conclusions The synthesis of HSP70 was prominently enhanced in the brain stem system in response to traumatic injury to eliminate the stress agents and maintain cellular protein homeostasis.When the injury was fatal, the synthesis of HSP70 was disturbed rendering this protective mechanism incompetent,and the brain stem dysfunction is resulted. The divorce of the expression of HSP70 and HSP70 mRNA can be interpreted as the sign of fatal injury of the neurons.