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首页> 外文期刊>Medical Gas Research >Isoflurane does not cause neuroapoptosis but reduces astroglial processes in young adult mice
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Isoflurane does not cause neuroapoptosis but reduces astroglial processes in young adult mice

机译：异氟烷不会引起神经细胞凋亡，但可以减少成年小鼠的星形胶质细胞生成过程

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Background Isoflurane, a volatile anesthetic widely used clinically, has been implicated to be both neuroprotective and neurotoxic. The claim about isoflurane causing neural apoptosis remains controversial. In this study, we investigated the effects of isoflurane exposures on apoptotic and anti-apoptotic signals, cell proliferation and neurogenesis, and astroglial processes in young adult mouse brains. Methods Sixty 6-week-old mice were randomly assigned to four anesthetic concentration groups (0 as control and 0.6%, 1.3%, and 2%) with four recovery times (2 h and 1, 6, and 14 d) after 2-h isoflurane exposure. Immunohistochemistry measurements of activated caspase-3 and Bcl-xl for apoptotic and anti-apoptotic signals, respectively, glial fibrillary acidic protein (GFAP) and vimentin for reactive astrocytosis, doublecortin (Dcx) for neurogenesis, and BrdU for cell proliferation were performed. Results Contrary to the previous conclusion derived from studies with neonatal rodents, we found no evidence of isoflurane-induced apoptosis in the adult mouse brain. Neurogenesis in the subgranule zone of the dentate gyrus was not affected by isoflurane. However, there is a tendency of reduced cell proliferation after 2% isoflurane exposure. VIM and GFAP staining showed that isoflurane exposure caused a delayed reduction of astroglial processes in the hippocampus and dentate gyrus. Conclusion Two-hour exposure to isoflurane did not cause neuroapoptosis in adult brains. The delayed reduction in astroglial processes after isoflurane exposure may explain why some volatile anesthetics can confer neuroprotection after experimental stroke because reduced glial scarring facilitates better long-term neuronal recoveries.
机译：背景技术异氟烷是一种临床上广泛使用的挥发性麻醉剂，被认为具有神经保护作用和神经毒性作用。关于异氟烷引起神经细胞凋亡的说法仍存在争议。在这项研究中，我们调查了异氟烷暴露对年轻成年小鼠大脑细胞凋亡和抗凋亡信号，细胞增殖和神经发生以及星形胶质过程的影响。方法将60只6周龄的小鼠随机分为四个麻醉浓度组（分别为0对照组和0.6％，1.3％和2％），在2次麻醉后2h，1，6和14 d恢复4次h异氟烷暴露。分别对活化的caspase-3和Bcl-xl的凋亡和抗凋亡信号，神经胶质纤维酸性蛋白（GFAP）和波形蛋白对反应性星形细胞增多症，双皮质素（Dcx）进行神经发生以及BrdU进行细胞增殖进行了免疫组织化学测量。结果与从对新生啮齿动物的研究得出的先前结论相反，我们没有发现异氟烷诱导成年小鼠脑细胞凋亡的证据。齿状回亚颗粒区的神经发生不受异氟烷影响。但是，异氟烷暴露于2％后，细胞增殖趋于减少。 VIM和GFAP染色显示，异氟烷暴露导致海马和齿状回中星形胶质过程的延迟减少。结论暴露于异氟烷两小时不会引起成人脑神经细胞凋亡。异氟烷暴露后星形胶质细胞过程的延迟减少可能解释了为什么某些挥发性麻醉药可在实验性中风后赋予神经保护作用，因为减少的神经胶质瘢痕形成有助于更好的长期神经元恢复。

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