JNK信号通路参与大鼠海马脑片氧糖剥夺损伤后的机制研究

王静; 刘华; 王建; 陆韦; 张骏

doi:10.13406/j.cnki.cyxb.002684

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JNK信号通路参与大鼠海马脑片氧糖剥夺损伤后的机制研究

神经病学 | 更新时间：2024-01-09

- JNK信号通路参与大鼠海马脑片氧糖剥夺损伤后的机制研究
- Mechanism of c-Jun N-terminal kinase signaling pathway involved in oxygen glucose deprivation injury in rat hippocampal slices
- 重庆医科大学学报 2021年46卷第5期页码：546-549
- 作者机构：
  
  遵义医科大学附属医院预防保健科,遵义,563000
- 作者简介：
- 基金信息：
  
  贵州省科学技术基金资助项目(编号：黔科合LH字20167476)
- DOI：10.13406/j.cnki.cyxb.002684
  中图分类号： R722.1
- 纸质出版日期：2021，
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王静, 刘华, 王建, 等. JNK信号通路参与大鼠海马脑片氧糖剥夺损伤后的机制研究[J]. 重庆医科大学学报, 2021,46(5):546-549.

Wang Jing, Liu Hua, Wang Jian, et al. Mechanism of c-Jun N-terminal kinase signaling pathway involved in oxygen glucose deprivation injury in rat hippocampal slices[J]. Journal of Chongqing Medical University, 2021,46(5):546-549.
王静, 刘华, 王建, 等. JNK信号通路参与大鼠海马脑片氧糖剥夺损伤后的机制研究[J]. 重庆医科大学学报, 2021,46(5):546-549. DOI： 10.13406/j.cnki.cyxb.002684.

Wang Jing, Liu Hua, Wang Jian, et al. Mechanism of c-Jun N-terminal kinase signaling pathway involved in oxygen glucose deprivation injury in rat hippocampal slices[J]. Journal of Chongqing Medical University, 2021,46(5):546-549. DOI： 10.13406/j.cnki.cyxb.002684.

摘要

目的：探讨c-Jun氨基末端激酶（c-Jun N-terminal kinase，JNK）参与大鼠离体脑片氧糖剥夺后的神经损伤机制。方法：出生后7 d的SD大鼠海马脑片制备，实验分为正常对照组、模型组及抑制剂组。正常组不经过氧糖剥夺（oxygen glucose deprivation，OGD）处理；模型组经OGD处理30 min；抑制剂组经OGD处理30 min的同时加用10 μmol/L SP600125。Wesern blot检测不同组别海马脑片的磷酸化JNK（phosphorylated-JNK，p-JNK）水平；全细胞膜片钳电流钳模式检测不同组别海马CA1区神经元的电位变化；此外，检测不同组别海马脑片乳酸脱氢酶的释放情况。结果： OGD 30 min后JNK磷酸化水平明显升高，同时，“静息状态”下神经元的电位绝对值下降而乳酸脱氢酶（lactic dehydrogenase，LDH）的释放水平升高，SP600125可明显抑制其磷酸化并使得神经元电位绝对值回升及抑制LDH释放（P<0.05）。结论：抑制JNK信号通路的过度激活，可减轻大鼠海马脑片OGD后神经损伤，其机制可能与调控神经元“静息状态”下的电位及LDH的释放有关。

Abstract

Objective: To investigate the nerve injury mechanism of c-Jun N-terminal kinase (JNK) in in vitro rat brain slices after oxygen glucose deprivation (OGD). Methods: The hippocampal slices of sprague dawley (SD) rats (7 days after birth) were prepared. Rats were divided into the normal control group

the model group and the inhibitor group. Brain slices in the normal group were not treated with OGD

in the model group were treated with OGD for 30 minutes

and in the inhibitor group were treated with OGD for 30 minutes and treated with 10 μmol/L SP600125.Levels of phosphorylated JNK (p-JNK) of hippocampal slices in different groups were detected by Western blot

potential changes of neurons of CA1 region in different groups were detected by whole cell patch clamp in current clamp mode

and the lactate dehydrogenase (LDH) releasing of hippocampal slices in different groups were also detected. Results: After 30 minutes of OGD

the phosphorylation level of JNK was significantly increased. Meanwhile

the potential absolute value of neurons in "resting state" was decreased

while the releasing level of LDH was increased. In addition

SP600125 was able to inhibit the phosphorylation of JNK

so as to recover the potential absolute value of neurons and inhibit the releasing of LDH (P<0.05). Conclusion: Inhibiting the over-activation of JNK signaling pathway can alleviate the neurological damage after OGD in rat hippocampal slices

and its mechanism may relate to the regulation of neuronal electrical state in "resting state" and LDH releasing.

关键词

c-Jun氨基末端激酶海马脑片氧糖剥夺膜片钳乳酸脱氢酶

Keywords

c-Jun N-terminal kinasehippocampal slicesoxygen glucose deprivationpatch clamplactate dehydrogenase

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