原儿茶酸对七氟醚诱导的小鼠神经元凋亡、炎症和氧化应激的保护作用。
Protective role of protocatechuic acid in sevoflurane-induced neuron apoptosis, inflammation and oxidative stress in mice.
机构信息
Department of Anesthesiology, General Hospital of Ningxia Medical University, Yinchuan, Ningxia, China.
Department of Ultrasound, General Hospital of Ningxia Medical University, Yinchuan, Ningxia, China.
出版信息
Restor Neurol Neurosci. 2020;38(4):323-331. doi: 10.3233/RNN-201022.
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 to explore 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.
背景
在新生小鼠中，通过鼻腔吸入的七氟醚作为麻醉剂，会引发神经元凋亡、炎症和氧化损伤，从而损害生命后期中枢神经系统的认知功能。
目的
本研究旨在探讨原儿茶酸（PCA）对改善新生小鼠七氟醚诱导的神经毒性的潜在神经保护作用。
方法
雄性小鼠在连续 6 小时 3%七氟醚处理前半小时用 PCA（10 或 20mg/kg）预处理。通过 TUNEL 染色检测凋亡细胞并记录其数量。通过 ELISA 评估白细胞介素-1β（IL-1β）、白细胞介素-18（IL-18）和肿瘤坏死因子-α（TNF-α）的蛋白表达。分析 Western blot 和 Morris 水迷宫测试结果。
结果
TUNEL 发现，用 PCA（20mg/kg）处理后，七氟醚处理的神经元凋亡明显减少。蛋白 Caspase-3 的表达在 SEV+PCA（20mg/kg）组中发生显著变化。ELISA 分析显示，与 SEV+PCA（10mg/kg）组相比，SEV+PCA（20mg/kg）组中 IL-18 和 TNF-α 的水平明显降低。只有在 SEV+PCA（20mg/kg）组中，MDA、ROS 和 SOD 水平才明显降低，而 IL-1β 水平在 SEV+PCA 两组（10 或 20mg/kg）中均降低。
结论
我们的研究结果表明，PCA 预处理可显著减轻新生小鼠大脑海马区的凋亡、炎症和氧化应激，提示 PCA 作为一种新型治疗药物，可用于治疗七氟醚麻醉诱导的神经行为功能障碍。
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