Objective:To research the effects of decompressive craniectomy on traumatic brain injury by investigating the changes of brain edema, the expression of AQP-4 in Rats. Method:The experimental TBI model was established by bumpiness of free falling body according to Feeney’s. Three groups were investigated:sham-operated group(SO),control group(C)and decompressive craniectomy group(DC). Decompressive craniectomy was performed at injury side immediately after brain insult. All animals were killed 6,12,24,72,120,168 h later. The rat brain tissue of injury side were examined for water content(wet/dry weight)and protein expression of AQP-4(western blot)respectively. Result:After TBI,water content of brain tissue and the protein expression of AQP-4 in injury region began to increase after brain insult. They reached summit at 24 h after insult,afterward dropped grdualaly. There was significantly positive correlation between expression of AQP-4 protein and the change of brain water content. Compared with the control group,brain water content and the expression of AQP-4 protein were decreased in the decompressive craniectomy group. Conclusion:The change of AQP-4 protein exression are closely related to the formation and development of brain edema during the early stage after traumatic brain injury. The early up-regulated expression of AQP-4 may increase the level of brain edema after the brain injury. And decompressive craniectomy has protective effects on traumatic brain injury by the mechanism of decreasing the expression of AQP-4 and thereby alleviating brain edema.%目的：研究去骨瓣减压术对大鼠创伤性脑损伤后脑水肿、水孔蛋白-4（AQP-4）表达的影响。方法：应用改良Feeney’s自由落体脑损伤打击装置制成大鼠创伤性脑损伤模型，分为假手术组（SO组）、对照组（C组）及去骨瓣减压组（DC组），各组在损伤后再分为6、12、24、72、120 h及168 h等6个时间点断头取脑损伤区组织。分别利用干湿重量法测量脑组织含水量和Western-Blot检测AQP-4蛋白的表达。结果：大鼠去骨瓣减压组脑组织含水量及AQP-4蛋白表达呈现先升高后降低的趋势，于伤后24 h达高峰后逐渐下降。与C组相比，上述指标含量均有所下降：脑组织含水量在24、120、168 h差异有统计学意义（P<0.05），72 h差异有高度统计学意义（P<0.01）；AQP-4蛋白表达在12、120 h时间点有统计学意义（P<0.05），24、168 h时有高度统计学意义（P<0.01）。结论：创伤后大鼠脑组织脑水肿与AQP-4表达上调密切相关；去骨瓣减压术可减轻脑水肿，减缓AQP-4表达。该手术对创伤性脑损伤的保护机制可能与减缓AQP-4蛋白表达，从而减轻脑水肿和继发性脑损伤，保护脑组织有关。
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