Croci Davide, Nevzati Edin, Danura Hiroki, Schöpf Salome, Fandino Javier, Marbacher Serge, Muroi Carl
Department of Neurosurgery, Kantonsspital Aarau, Aarau, Switzerland -
Neuro Lab, Research Group for Experimental Neurosurgery and Neurocritical Care, Department of Intensive Care Medicine, University Hospital and University of Bern, Bern, Switzerland -
J Neurosurg Sci. 2019 Jun;63(3):245-250. doi: 10.23736/S0390-5616.16.03876-5. Epub 2016 Oct 19.
In subarachnoid hemorrhage (SAH), occurrence of cerebral vasospasm (CVS) mediated by endothelin (ET)-1 might be a result of a compartmental inflammatory response with interleukin (IL)-6 release. We aim to investigate the relationship between ET-1 and IL-6 in association of CVS.
A total of 24 New Zealand white rabbits where randomly allocated into 3 groups: SAH (N.=10), IL-6 (N.=10), and sham (N.=4). SAH was induced by a closed cranium extracranial-intracranial shunt model. In the IL-6 group, IL-6 was injected into the cisterna magna. CVS of the basilar artery was assessed by digital subtraction angiography. IL-6 and ET-1 concentrations were measured using enzyme-linked immunosorbent assay. Neuronal damage was assessed by terminal deoxynucleotidyl transferase dUTP nick end labeling.
A significant increase between baseline (day 0) and follow-up (day 3) was found in CSF IL-6 levels of animals in the SAH and IL-6 group. There was a statistically significant correlation between IL-6 and ET-1 levels in the CSF (Pearson's r=0.454, P=0.003). CVS at day 3 was more pronounced in the SAH than in the IL-6 group: 26.0 ±7.2 % and 16.7 ±5.0 % respectively. TUNEL positive apoptotic neurons in the hippocampal formation were present in the SAH group and in a lesser degree in the IL-6 group.
The results indicate that IL-6 triggered CVS after SAH is ET-1 dependent. IL-6 may be a target for new therapeutic approaches.
在蛛网膜下腔出血（SAH）中，由内皮素（ET）-1介导的脑血管痉挛（CVS）的发生可能是伴有白细胞介素（IL）-6释放的局部炎症反应的结果。我们旨在研究ET-1与IL-6在CVS关联中的关系。
将总共24只新西兰白兔随机分为3组：SAH组（n = 10）、IL-6组（n = 10）和假手术组（n = 4）。通过闭合颅骨的颅外-颅内分流模型诱导SAH。在IL-6组中，将IL-6注入枕大池。通过数字减影血管造影评估基底动脉的CVS。使用酶联免疫吸附测定法测量IL-6和ET-1浓度。通过末端脱氧核苷酸转移酶dUTP缺口末端标记评估神经元损伤。
SAH组和IL-6组动物的脑脊液IL-6水平在基线（第0天）和随访（第3天）之间显著升高。脑脊液中IL-6和ET-1水平之间存在统计学显著相关性（Pearson相关系数r = 0.454，P = 0.003）。SAH组第3天的CVS比IL-6组更明显：分别为26.0±7.2%和16.7±5.0%。SAH组海马结构中存在TUNEL阳性凋亡神经元，IL-6组程度较轻。
结果表明，SAH后IL-6引发的CVS依赖于ET-1。IL-6可能是新治疗方法的靶点。
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