局灶性脑低温处理对大鼠创伤性脑损伤模型的保护作用

目的探讨局灶性低温处理对SD大鼠创伤性脑损伤（TBI）模型的保护作用并探讨其相关机制。 方法将15只雄性SD大鼠随机平均分成假手术组（sham），非冷却组（non-cooling）和冷却组（cooling）。Non-cooling组和cooling组制作TBI模型，3组实验同步进行，创伤后低温处理3 h，复温3 h，过程中检测大鼠血气、皮层脑电。复温结束处死大鼠后，对脑组织进行TTC和HE染色以评价脑死亡和脑水肿情况，Western blot检测相关机制蛋白表达情况。 结果Sham组和non-cooling组受外部刺激脑组织代谢升高，cooling组较其他组脑组织代谢低，TTC和HE染色显示cooling组脑死亡的面积和细胞死亡数量均少于non-cooling组，差异均具有统计学意义（P<0.05）。大鼠TBI后局灶性低温处理能显著降低大脑皮层的癫痫样棘波，在回温时这种不完全抑制持续存在，且低温处理降低了GABA_B1R蛋白的表达，差异均具有统计学意义（P<0.05）。Cooling组的脑水肿情况较non-cooling组轻，且cooling组AQP4蛋白表达降低，差异均具有统计学意义（P<0.05）。 结论局灶性低温处理对TBI大鼠具有保护作用，能显著减轻TBI引起的脑水肿，抑制大脑皮层的癫痫样棘波，具体机制可能分别与GABA_B1R和AQP4相关。为临床治疗TBI提供了一种更加安全、简单有效的方法。

Protective effect of focal cerebral hypothermia on traumatic brain injury model

ObjectiveTo explore the protective effect of focal cerebral hypothermia on traumatic brain injury (TBI) model in SD rats and the underlying mechanisms. MethodsFifteen male SD rats were randomly divided into a sham group, a non-cooling group, and a cooling group, with 5 in each group. The TBI model was made by non-cooling group and cooling group. Three groups of experiments were performed simultaneously. After trauma, the mice were treated with hypothermia for 3 h and rewarmed for 3 h. Rat blood gas and cortical brain electricity were detected during the experiment. Rats were sacrificed at the end of rewarming, and brain tissue was stained with TTC or HE to evaluate brain death. The cerebral edema was evaluated and the expression of related proteins was detected by Western blot. ResultsSham group and non-cooling group were increased in metabolism by externally stimulated brain tissue, and metabolism of cooling group is low (P<0.05). TTC and HE staining showed that the area of brain death and cell death in the cooling group were less than those in the non-cooling group (P<0.05). Focal hypothermia after TBI significantly reduces epileptic spikes in the cerebral cortex (P<0.05). This incomplete inhibition persists during rewarming, and hypothermia treatment reduces the expression of GABA_B1R (P<0.05). Brain edema in the cooling group was significantly improved compared with the non-cooling group (P<0.05) and expression of AQP4 protein in the cooling group was significantly lower (P<0.05). ConclusionFocal hypothermia has a protective effect on TBI rats, which significantly reduce brain edema caused by TBI and inhibit epileptic spikes in the cerebral cortex. The underlying mechanism may be related to GABA_B1R and AQP4, respectively. It provides a safer, simpler and more effective method for clinical treatment of TBI.