妊娠中期罗哌卡因联合舒芬太尼麻醉对SD模型子代脑源性神经营养因子表达和认知功能的影响

doi:10.3969/j.issn.1006-6233.2024.05.013

摘要
图/表
参考文献
相关文章 (15)

全文: PDF (2262 KB) HTML (1 KB)
输出: BibTeX | EndNote (RIS)

摘要 目的: 探讨妊娠中期罗哌卡因联合舒芬太尼麻醉对SD模型子代脑源性神经营养因子表达和认知功能的影响。方法: 本研究假设怀孕期间的母体跑步机运动可以防止罗哌卡因联合舒芬太尼引起的神经毒性。在第一个实验中,怀孕大鼠在妊娠(G)第14天暴露于舒芬太尼(0.25μg/μL)+罗哌卡因(0.125μg/μL)混合液 100μL(R&G),或在 G13,G14和 G15上连续暴露(R&Gx3)。在第二个实验中,运动组的怀孕大鼠在整个怀孕期间被迫在跑步机上每天跑60min。TrkB 拮抗剂 ANA-12被用来研究脑源性神经营养因子(brain-derived neurotrophic factor,BDNF)/TrkB信号通路是否参与了母亲运动所提供的神经保护。结果: 重复而非单一暴露于罗哌卡因联合舒芬太尼会导致胎儿脑组织和出生后海马中组蛋白乙酰化和BDNF表达的降低。伴随着树突棘数量的减少,空间依赖性学习和记忆功能障碍受损。母体运动减轻了这些影响,但TrkB拮抗剂ANA-12消除了母体运动的有益影响。结论: 妊娠大鼠在妊娠中期多次(而非单次)接触罗哌卡因联合舒芬太尼会导致后代长期学习和记忆功能障碍。母体运动通过增强组蛋白乙酰化和激活下游BDNF/TrkB信号传导以改善产后神经认知障碍。

	服务

	把本文推荐给朋友
	加入我的书架
	加入引用管理器
	E-mail Alert
	RSS
	作者相关文章

关键词 ：妊娠中期, 罗哌卡因, 舒芬太尼, 脑源性神经营养因子, 认知功能

Abstract：Objective: To investigate the effects of combined ropivacaine and sufentanil anesthesia in mid-pregnancy on progeny brain-derived neurotrophic factor (BDNF) expression and cognitive function in SD rats. Methods: The study hypothesized that maternal treadmill exercise during pregnancy could prevent neurotoxicity induced by ropivacaine and sufentanil. In the first experiment, pregnant rats were exposed to a 100 μL mixture of sufentanil (0.25 μg/μL) and ropivacaine (0.125 μg/μL) (R&G) on gestational (G) day 14, or were exposed continuously on G13, G14, and G15 (R&Gx3). In the second experiment, pregnant rats in the exercise group were forced to run on a treadmill for 60 minutes daily throughout pregnancy. The TrkB antagonist ANA-12 was used to investigate whether the BDNF/TrkB signaling pathway was involved in the neuroprotection provided by maternal exercise. Results: Repeated but not single exposure to ropivacaine and sufentanil led to a decrease in histone acetylation and BDNF expression in fetal brain tissue and postnatal hippocampus. Spatial learning and memory impairments were compromised, accompanied by a reduction in dendritic spine number. Maternal exercise mitigated these effects, but the TrkB antagonist ANA-12 abolished the beneficial effects of maternal exercise. Conclusion: Multiple (but not single) exposures to ropivacaine and sufentanil in mid-pregnancy in pregnant rats lead to long-term learning and memory impairments in offspring. Maternal exercise improves postnatal neurocognitive deficits by enhancing histone acetylation and activating downstream BDNF/TrkB signaling.

Key words： Mid-pregnancy Ropivacaine Sufentanil Brain-derived neurotrophic factor Cognitive function

基金资助:2020年度河北省医学科学研究课题计划,(编号:20200258)

通讯作者: 王金保

引用本文:

底妍, 李立函, 焦姗姗, 张坤, 郝书航, 王金保. 妊娠中期罗哌卡因联合舒芬太尼麻醉对SD模型子代脑源性神经营养因子表达和认知功能的影响[J]. 河北医学, 2024, 30(5): 773-780.
DI Yan, LI Lihan, JIAO Shanshan, et al. Effect of Combined Ropivacaine and Sufentanil Anesthesia in Mid-Pregnancy on Progeny Brain-Derived Neurotrophic Factor Expression and Cognitive Function in SD Rats. HeBei Med, 2024, 30(5): 773-780.

链接本文:

http://www.hbyxzzs.cn/CN/10.3969/j.issn.1006-6233.2024.05.013 或 http://www.hbyxzzs.cn/CN/Y2024/V30/I5/773

[1] Andropoulos DB,Greene MF.Anesthesia and developing brains - implications of the FDA warning[J].N Engl Med,2017,376(10):905-907.
[2] Murphy KL,Baxter MG.Long-term effects of neonatal single or multiple isoflurane exposures on spatial memory in rats[J].Front Neurol,2013(4):87.
[3] Martinez-Levy GA,Cruz-Fuentes CS.Genetic and epigenetic regulation of the brain-derived neurotrophic factor in the central nervous system[J].Yale Biol Med,2014,87(2):173-186.
[4] Gao LL,Wang ZH,Mu YH,et al.Emodin promotes autophagy and prevents apoptosis in sepsis-associated encephalopathy through activating BDNF/TrkB signaling[J].Pathobiology,2022,89(3):135-145.
[5] Xu Y,Tian Y,Tian Y,et al.Autophagy activation involved in hypoxic-ischemic brain injury induces cognitive and memory impairment in neonatal rats[J].Neurochem,2016,139(5):795-805.
[6] Zheng H,Dong Y,Xu Z,et al.Sevoflurane anesthesia in pregnant mice induces neurotoxicity in fetal and offspring mice[J].Anesthesiology,2013,118(3):516-26.
[7] Lee J,Cho JY,Oh SD,et al.Maternal exercise reduces hyperthermia-induced apoptosis in developing mouse brain[J].Int Hyperthermia,2011,27(5):445-452.
[8] Andropoulos DB,Greene MF.Anesthesia and developing brains - implications of the FDA warning[J].N Engl Med,2017,376(10):905-907.
[9] Li X,Zhang J,Li D,et al.Astrocytic ApoE reprograms neuronal cholesterol metabolism and histone-acetylation-mediated memory[J].Neuron,2021,109(6):957-970.
[10] Peixoto L,Abel T.The role of histone acetylation in memory formation and cognitive impairments[J].Neuropsychopharmacology,2013,38(1):62-76.
[11] Martynyuk AE,Ju LS,Morey TE,et al.Neuroendocrine,epigenetic,and intergenerational effects of general anesthetics[J].World Psychiatry,2020,10(5):81-94.
[12] Kowianski P,Lietzau G,Czuba E,et al.BDNF:a key factor with multipotent impact on brain signaling and synaptic plasticity[J].Cell Mol Neurobiol,2018,38(3):579-593.
[13] Wang D,Li B,Wu Y,et al.The Effects of maternal atrazine exposure and swimming training on spatial learning memory and hippocampal morphology in offspring male rats via PSD95/NR2B signaling pathway[J].Cell Mol Neurobiol,2019,39(7):1003-1015.
[14] Sun H,Zhang X,Kong Y,et al.Maternal separation-induced histone acetylation correlates with BDNF-programmed synaptic changes in an animal model of PTSD with sex differences[J].Mol Neurobiol,2021,58(4):1738-1754.
[15] Gorgij E,Fanaei H,Yaghmaei P,et al.Treadmill exercise during pregnancy decreased vulnerability to neonatal hypoxia-ischemia through reducing inflammation and increasing antiapoptotic gene expressions and antioxidant capacity in rats[J].Stroke Res Treat,2021(2021):5512745.