The effect of ecdysterone on cerebral vasospasm following experimental subarachnoid hemorrhage in vitro and in vivo.
The effect of ecdysterone on cerebral vasospasm following experimental subarachnoid hemorrhage in vitro and in vivo.
复制标题
蜕皮甾酮对体内外实验性蛛网膜下腔出血脑血管痉挛的影响
DOI：
10.1179/174313208x297986
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发表时间：
2008-07
影响因子：
1.9
通讯作者：
Feng H
中科院分区：
文献类型：
--
作者：
Tang WH;Chen Z;Liu Z;Zhang JH;Xi G;Feng H
摘要目的：脑血管痉挛一直是颅内动脉瘤破裂后可怕的并发症。世界范围内的努力导致了许多有希望的实验性治疗，但没有一个被证实在临床试验中有效。蜕皮甾酮是一种昆虫类固醇激素。我们前期的研究表明蜕皮甾酮在体外有预防脑血管痉挛的作用。即使在所有这些工作之后，也很少尝试测试蜕皮甾酮对血管外膜成纤维细胞（VAF）增殖的影响，该过程已知在各种致病性血管病症中起重要作用。因此，我们验证了蜕皮甾酮可以影响VAF特征并对SAH诱导的脑血管痉挛有影响的假设。方法：体外实验采用100 μM的OxyHb模拟临床情况。观察了OxyHb对培养的主动脉平滑肌细胞增殖和迁移的影响。在体内实验中，将20只家兔分为4组：对照组、SAH组、SAH/尼莫地平组和SAH/蜕皮甾酮组。观察SAH后神经功能和脑血管造影的变化。结果：OxyHb作用24 h后，血管外膜成纤维细胞增殖明显增加。蜕皮甾酮联合治疗明显类似于抑制增殖。细胞周期分析表明蜕皮甾酮抑制血管外膜成纤维细胞从G1期向S期的转化。迁移实验结果表明，100 μM OxyHb可明显促进血管外膜成纤维细胞迁移，蜕皮甾酮可减弱这种作用。尼莫地平组和蜕皮甾酮组神经功能缺损、脑血管痉挛和基底动脉结构改变均较尼莫地平组减轻。结论：蜕皮甾酮可影响SAH后血管外膜成纤维细胞的特性，减轻SAH后血管痉挛。
Abstract Objectives: Cerebral vasospasm has been the dreaded complication of ruptured intracranial aneurysms. Worldwide effort has led to many promising experimental treatments but none was confirmed to be effective in clinical trials. Ecdysterone is an insect steroid hormone. Our previous study showed that ecdysterone might prevent cerebral vasospasm in vitro. Even after all these works, rare attempts have been made to test the effect of ecdysterone on vascular adventitial fibroblast (VAF) proliferation, a process known to play an important role in various pathogenic vascular conditions. Thus, we tested the hypothesis that ecdysterone could affect VAF characteristics and have an effect on SAH induced cerebral vasospasm. Methods: OxyHb of 100 μM was used in the in vitro study to mimic the clinical situation. The effect of OxyHb on the cell proliferation and migration of cultured aortic smooth muscle cells was investigated. In the in vivo study, 20 rabbits were equally divided into four groups: control group, SAH group, SAH/nimodipine group and SAH/ecdysterone group. Changes in neurological function and cerebral angiograms were observed after SAH. Results: OxyHb increased the proliferation of vascular adventitial fibroblasts at 24 hours. Ecdysterone co-treatment was apparently similar to the suppression of proliferation. Cell cycle analysis indicated that ecdysterone inhibited the progression of vascular adventitial fibroblasts from G1 to S. The results of the migration assay showed that 100 μM OxyHb obviously prompted vascular adventitial fibroblast migration and that ecdysterone would attenuate this effect. In the SAH/nimodipine and SAH/ecdysterone groups, neurological deficit, cerebral vasospasm and structural changes in basilar artery were alleviated with nimodipine or ecdysterone treatment. Conclusion: Ecdysterone could affect vascular adventitial fibroblast characteristics and attenuate vasospasm after SAH.