Tu Y, Fu J, Wang J, Fu G, Wang L, Zhang Y
Experimental Surgery Department, Tangdu Hospital, The Fourth Military Medical University, Xi'an, China.
J Int Med Res. 2012;40(3):1089-98. doi: 10.1177/147323001204000328.
Brain oedema is a major cause of clinical deterioration and death following brain trauma; cellular mechanisms involved in its development remain elusive. This study investigated the role of extracellular matrix metalloproteinase inducer (EMMPRIN) in brain oedema.
The monofilament puncture model was used to induce subarachnoid haemorrhage. Adult male Sprague-Dawley rats were divided into five groups (n = 20 per group): sham-operated, sacrificed immediately after surgery (sham group); sacrificed 12, 24 or 72 h after subarachnoid haemorrhage induction (SAH-12, SAH-24 and SAH-72 groups, respectively); treated with EMMPRIN inhibitor immediately after subarachnoid haemorrhage, sacrificed at 24 h (SAH-inhibition group). Mean brain water content, and EMMPRIN mRNA and protein levels, were determined.
Compared with the sham group, mean brain water content, EMMPRIN mRNA and protein levels in the SAH-12, SAH-24 and SAH-72 groups increased rapidly and significantly (maximal at 24 h). EMMPRIN inhibition significantly reduced mean brain water content and EMMPRIN mRNA and protein levels in the SAH-inhibition group, compared with the SAH-24 group.
EMMPRIN upregulation may be important in the formation of brain oedema; inhibition of EMMPRIN activity may provide a potential approach to reduce oedema after subarachnoid haemorrhage.
脑水肿是脑外伤后临床病情恶化和死亡的主要原因；其发展过程中涉及的细胞机制仍不清楚。本研究调查了细胞外基质金属蛋白酶诱导剂（EMMPRIN）在脑水肿中的作用。
采用单丝穿刺模型诱导蛛网膜下腔出血。成年雄性Sprague-Dawley大鼠分为五组（每组n = 20）：假手术组，术后立即处死（假手术组）；蛛网膜下腔出血诱导后12、24或72小时处死（分别为SAH-12、SAH-24和SAH-72组）；蛛网膜下腔出血后立即用EMMPRIN抑制剂治疗，24小时处死（SAH抑制组）。测定平均脑含水量以及EMMPRIN mRNA和蛋白水平。
与假手术组相比，SAH-12、SAH-24和SAH-72组的平均脑含水量、EMMPRIN mRNA和蛋白水平迅速且显著升高（在24小时达到峰值）。与SAH-24组相比，EMMPRIN抑制显著降低了SAH抑制组的平均脑含水量以及EMMPRIN mRNA和蛋白水平。
EMMPRIN上调可能在脑水肿形成中起重要作用；抑制EMMPRIN活性可能为减少蛛网膜下腔出血后的水肿提供一种潜在方法。
