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Protective role of protocatechuic acid in sevoflurane-induced neuron apoptosis, inflammation and oxidative stress in mice
Restorative Neurology and Neuroscience ( IF 1.9 ) Pub Date : 2020-08-06 , DOI: 10.3233/rnn-201022
Yuhua Gao 1 , Liping Ma 1 , Tao Han 2 , Meng Wang 1 , Dongmei Zhang 1 , Yana Wang 3
Affiliation  

Background:In neonatal mice, sevoflurane, inspired through the nasal cavity to act as anesthesia, triggers neuronal apoptosis, inflammation and oxidative injury that can hamper cognitive functions in the growth of the central nervous system in the later stages of life. Objective:Our study aimed toexplore the potential neuroprotective effects of protocatechuic acid (PCA) to ameliorate neonatal sevoflurane-induced neurotoxicity. Methods:Male mice were pretreated with PCA (10 or 20 mg/kg) for half an hour before continuous treatment for 6 h with 3 % sevoflurane. TUNEL staining was performed to examine the apoptotic cells to record their count. ELISA was performed to evaluate the expressions of the proteins - IL-1β, IL-18 and TNF-α. Analysis of the Western blot and test of the Morris maze was determined and the results analyzed. Results:TUNEL findings assay showed a significant reduction with sevoflurane in neuronal apoptosis treated with PCA at 20 mg/kg. The expression of protein Caspase-3 showed significant changes in the group SEV + PCA (20 mg/kg). ELISA analysis showed that the levels of IL-18 and TNF-α were significantly reduced in the SEV + PCA (20 mg/kg) group as compared to SEV + PCA (10 mg/kg) group. MDA, ROS and SOD levels were noted to decrease significantly only in the SEV + PCA group (20 mg/kg) while IL-1β levels decreased in both SEV + PCA groups (10 or 20 mg/kg) respectively. Conclusions:Our findings imply that apoptosis, inflammation, and oxidative stress in the hippocampal region of neonatal mouse brain were significantly reduced by pre-treatment with PCA before sevoflurane exposure. Therefore, suggesting a role for PCA as a novel therapeutic agent in the treatment of sevoflurane anesthesia-induced neurobehavioral dysfunction.

中文翻译:

原儿茶酸在七氟醚诱导的小鼠神经元凋亡,炎症和氧化应激中的保护作用

背景:在新生小鼠中,七氟醚通过鼻腔激发而起麻醉作用,触发神经元凋亡,炎症和氧化损伤,这些损伤会妨碍生命后期中枢神经系统生长的认知功能。目的:我们的研究旨在探讨原儿茶酸(PCA)对减轻七氟醚对新生儿神经毒性的潜在神经保护作用。方法:雄性小鼠用PCA(10或20 mg / kg)预处理半小时,然后用3%的七氟醚连续处理6 h。进行TUNEL染色以检查凋亡细胞以记录其计数。进行ELISA以评估蛋白质-IL-1β,IL-18和TNF-α的表达。测定蛋白质印迹分析和莫里斯迷宫测试,并分析结果。结果:TUNEL结果分析显示七氟醚在以20 mg / kg的PCA处理的神经元凋亡中显着减少。在SEV + PCA组(20 mg / kg)中,Caspase-3蛋白的表达显示出显着变化。ELISA分析显示,与SEV + PCA(10 mg / kg)组相比,SEV + PCA(20 mg / kg)组中IL-18和TNF-α的水平显着降低。注意到仅在SEV + PCA组(20 mg / kg)中MDA,ROS和SOD水平显着降低,而在SEV + PCA组(10或20 mg / kg)中IL-1β水平分别降低。结论:我们的研究结果表明,七氟醚暴露前用PCA预处理可显着减少新生小鼠大脑海马区的细胞凋亡,炎症和氧化应激。因此,
更新日期:2020-08-11
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