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| GM-1预处理减轻布比卡因诱导的N2a细胞凋亡 |
| Effect of GM-1 pretreatment reducing the apoptosis after bupivacaine-induced in N2a cells |
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| DOI：10.12089/jca.2021.03.013 |
| 中文关键词: 布比卡因 神经毒性 单唾液酸四己糖神经节苷脂 c-Jun氨基末端激酶；CCAAT/增强子结合蛋白同源蛋白 N2a细胞； 细胞凋亡 |
| 英文关键词: Bupivacaine Neurotoxicity Monosialoganglioside c-Jun N-terminal kinase CCAAT/enhancer binding protein homologous protein N2a cell Apoptosis |
| 基金项目:国家自然科学基金资助项目（81660623），广西研究生教育创新计划项目（YCSW2020117） |
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| 中文摘要: |
目的 研究单唾液酸四己糖神经节苷脂（GM-1）预处理对布比卡因诱导N2a细胞凋亡后对c-Jun氨基末端激酶（JNK ）、CCAAT/增强子结合蛋白同源蛋白（CHOP）表达的影响。
方法 体外培养小鼠神经母细胞瘤细胞 N2a细胞株，取对数生长期N2a细胞，将细胞随机分为四组：对照组（C组），N2a细胞无任何药物处理；GM-1组（G组），N2a细胞中加入GM-1 5 μmol/L处理24 h；布比卡因组（B组），N2a细胞中加入布比卡因900 μmol/L处理36 h；GM-1预处理组（GB组），GM-1 5 μmol/L预处理24 h后，N2a细胞中加入布比卡因900 μmol/L处理36 h。以倒置显微镜观察细胞形态学变化，采用TUNEL法检测细胞凋亡率，采用qRT-PCR法和Western blot法分别检测细胞内JNK和CHOP mRNA表达量及蛋白含量。
结果 与C组比较，B组和GB组细胞损伤形态明显加重，凋亡率明显升高，JNK和CHOP mRNA表达量及蛋白含量明显升高（P<0.05）。与B组比较， GB组细胞损伤形态明显减轻，凋亡率明显下降，JNK和CHOP mRNA表达量及蛋白含量明显降低（P<0.05）。
结论 GM-1预处理通过调控内质网应激凋亡途径中相关蛋白JNK和CHOP的表达，从而减少布比卡因诱导的细胞凋亡，减轻布比卡因引起的神经毒性。 |
| 英文摘要: |
Objective To measure the effect of expressions of c-JNK N-terminal kinase (JNK), CCAAT/enhancer binding protein homologous protein (CHOP) after monosialoganglioside (GM-1) pretreatment on bupivacaine-induced apoptosis in N2a cells.
Methods Mice nerve N2a cells cultured in vitro. Growing N2a cells were randomly divided into four groups: the control group (group C), N2a cells were treated without any drug; GM-1 group (group G), N2a cells were cultured with 5 μmol/L GM-1 for 24 hours; bupivacaine group (group B), N2a cells were treated with 900 μmol/L bupivacaine for 36 hours; GM-1 pretreatment group (group GB), N2a cells were pretreated with GM-1 for 24 hours and then added 900 μmol/L bupivacaine for 36 hours. Light Microscope was detected to observe the morphological changes of the cells of N2a. TUNEL assay was measured the apoptosis rate of N2a cells. Real-time polymerase chainreaction and Western blotting evaluated the expressions of JNK and CHOP. Each expreiment was repeated three times.
Results Compared with group C, N2a cells of groups B and GB were seriously damaged under the light microscope and the apoptosis rate was incresead, the mRNA and protein expressions of JNK and CHOP were significantly increased (P < 0.05). Compared with group B, N2a cells of group GB had less cell damage morphology, and the apoptosis rate was reduced, mRNA and protein expressions of JNK and CHOP were significantly reduced (P < 0.05).
Conclusion GM-1 pretreatment regulated the expression of JNK and CHOP in the apoptosis pathway of endoplasmic reticulum stress, thereby reducing bupivacaine-induced cell apoptosis and had a certain protective effect on bupivacaine-induced neurotoxicity in N2a cells. |
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