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本公众号每天分享一篇最新一期Anesthesia & Analgesia等SCI杂志的摘要翻译，敬请关注并提出宝贵意见 Dexmedetomidine alleviates neurogenesis damage following neonatal midazolam exposure in rats through JNK and P38 MAPK pathways 背景与目的 咪达唑仑是一种广泛应用的麻醉药，可抑制神经干细胞（NSCs）的增殖，并诱导新生儿神经细胞凋亡。右美托咪啶是临床麻醉中有效的辅助药物，可保护发育中的大脑免受挥发性麻醉药诱导产生的神经细胞凋亡的影响。右美托咪啶是否能保护咪达唑仑引起的神经发生损伤目前尚不清楚。本研究旨在阐明右美托咪啶对咪达唑仑诱导产生的神经损伤具有保护作用，并探讨其可能的机制。 方 法 分别用生理盐水、咪达唑仑和右美托咪啶联合咪达唑仑处理7日龄SD大鼠和培养的神经干细胞。分别于治疗后1、3、7d处死大鼠。使用Brdu法检测细胞增殖情况。MTT法测定细胞活力。分别采用免疫荧光染色和末端dUTP标记法(TUNEL)检测细胞凋亡。Western blotting检测p-JNK、p-P38和caspase-3蛋白表达水平。 结 果 咪达唑仑可降低脑室下区(SVZ)、海马颗粒下区(SGZ)和培养的NSCs的增殖、增加细胞凋亡。此外，咪达唑仑降低神经干细胞的存活率，增加p-JNK和p-P38蛋白的表达。右美托咪啶可减轻咪达唑仑对神经干细胞增殖、活力、凋亡及p-JNK、p-P38蛋白表达的影响。咪达唑仑和/或右美托咪啶对神经干细胞的分化无影响。 结 论 右美托咪啶通过JNK和P38 MAPK通路减轻咪达唑仑诱导产生的神经损伤。 原始文献摘要 Shan Lei,Pan Lu,Yang Lu,et al.Dexmedetomidine alleviates neurogenesis damage following neonatal midazolam exposure in rats through JNK and P38 MAPK pathways.ACS Chemical Neuroscience.2020,14:123–130 AIM:Midazolam, a widely used anesthetic, inhibits proliferation of neural stem cells (NSCs) and induces neuroapoptosis in neonates. Dexmedetomidine, an effective auxiliary medicine in clinical anesthesia, protects the developing brain against volatile anesthetic-induced neuroapoptosis. Whether dexmedetomidine protects against neurogenesis damage induced by midazolam remains unknown. This study aims to clarify the protective effect of dexmedetomidine on midazolam-induced neurogenesis damage and explore its potential mechanism. Methods:Postnatal 7-day-old Sprague-Dawley (SD) rats and cultured NSCs were treated with either normal saline, midazolam, or dexmedetomidine combined with midazolam. The rats were sacrificed at 1, 3, and 7 days after treatment. Cell proliferation was assessed by 5-bromodeoxyurdine (BrdU) incorporation. Cell viability was determined using MTT assay. Cell differentiation and apoptosis were detected by immunofluorescent staining and terminal dUTP nick-end labeling (TUNEL), respectively. The protein levels of p-JNK, p-P38, and cleaved caspase-3 were quantified using Western blotting. Result:Midazolam decreased cell proliferation and increased cell apoptosis in the subventricular zone (SVZ), the subgranular zone (SGZ) of the hippocampus, and cultured NSCs. Moreover, midazolam decreased cell viability and increased the expression of p-JNK and p-P38 in cultured NSCs. Co-treatment with dexmedetomidine attenuated midazolam-induced changes in cell proliferation, viability, apoptosis, and protein expression of p-JNK and p-P38 in cultured NSCs. Midazolam and dexmedetomidine did not affect the differentiation of the cultured NSCs. Conclusion:These results indicate that dexmedetomidine alleviated midazolam-induced neurogenesis damage via JNK and P38 MAPK pathways. 麻醉学文献进展分享 贵州医科大学高鸿教授课题组 翻译：唐剑 编辑：冯玉蓉 审校：王贵龙 |
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