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研究苏伽[玛]德ex 对 C6 细胞系谷氨酸诱导的神经毒性的影响及一氧化氮和氧化应激途径的作用。

Investigation of the effect of sugammadex on glutamate-induced neurotoxicity in C6 cell line and the roles played by nitric oxide and oxidative stress pathways.

机构信息

Anestezi ve Yoğun Bakım, Ankara Şehir Hastanesi, Ankara, Turkey.

Department of Pharmacology, School of Pharmacy, Cumhuriyet University, Sivas, Turkey.

出版信息

Fundam Clin Pharmacol. 2023 Aug;37(4):786-793. doi: 10.1111/fcp.12890. Epub 2023 Mar 14.

DOI:10.1111/fcp.12890
PMID:36880372
Abstract

This experiment was intended to evaluate the effect of sugammadex on the cytotoxicity induced by glutamate, involving the nitric oxide and oxidative stress pathways. C6 glioma cells were used in the study. Glutamate was given to cells in the glutamate group for 24 h. Sugammadex at different concentrations was given to cells in the sugammadex group for 24 h. Cells in the sugammadex + glutamate group were pre-treated with sugammadex at various concentrations for 1 h and then exposed to glutamate for 24 h. XTT assay was used to assess cell viability. Levels of nitric oxide (NO), neuronal nitric oxide synthase (nNOS), total antioxidant (TAS), and total oxidant (TOS) in the cells were calculated using commercial kits. Apoptosis was detected by TUNEL assay. Sugammadex at concentrations of 50 and 100 μg/mL significantly enhanced the cell viability in C6 cells after the cytotoxicity induced by glutamate (p < 0.001). Moreover, sugammadex considerably decreased the levels of nNOS NO and TOS and the number of apoptotic cells and increased the level of TAS (p < 0.001). Sugammadex has protective and antioxidant properties on cytotoxicity and could be an effective supplement for neurodegenerative diseases such as Alzheimer and Parkinson if further research in vivo supports this claim.

摘要

本实验旨在评估氨甲环酸对谷氨酸诱导的细胞毒性的影响,涉及一氧化氮和氧化应激途径。研究中使用 C6 神经胶质瘤细胞。谷氨酸组细胞给予谷氨酸 24 小时。氨甲环酸组细胞给予不同浓度的氨甲环酸 24 小时。氨甲环酸+谷氨酸组细胞先用不同浓度的氨甲环酸预处理 1 小时,然后暴露于谷氨酸 24 小时。采用 XTT 法检测细胞活力。采用商业试剂盒测定细胞中一氧化氮(NO)、神经元型一氧化氮合酶(nNOS)、总抗氧化(TAS)和总氧化(TOS)水平。TUNEL 法检测细胞凋亡。谷氨酸诱导细胞毒性后,50 和 100μg/ml 的氨甲环酸显著提高 C6 细胞的细胞活力(p<0.001)。此外,氨甲环酸可显著降低 nNOS、NO 和 TOS 水平及凋亡细胞数量,增加 TAS 水平(p<0.001)。氨甲环酸对谷氨酸诱导的细胞毒性具有保护和抗氧化作用,如果进一步的体内研究支持这一说法,它可能是阿尔茨海默病和帕金森病等神经退行性疾病的有效补充治疗药物。

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