| 引用本文:王春玲1，罗宁2，蒋媛静2，蒙冰2，左曜玮1，李昌海1，文晓东2.基于CaMkkβ/AMPK通路介导线粒体自噬探讨敛肝熄风止颤方的神经保护机制[J].世界中医药,2021,(05):. |
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| 基于CaMkkβ/AMPK通路介导线粒体自噬探讨敛肝熄风止颤方的神经保护机制 |
| Study on the Neuroprotective Mechanism of Lianggan Xifeng Zhichan Formula Based on Mitochondrial Autophagy Mediated by CaMkkβ/AMPK Pathway |
| 投稿时间：2019-11-30 |
| DOI：10.3969/j.issn.1673-7202.2021.05.015 |
| 中文关键词: 帕金森病 敛肝熄风止颤方 机制 线粒体 自噬 神经保护 CaMkkβ/AMPK通路 |
| English Keywords:Parkinson's disease Linggan Xifeng Zhichan Formula Mechanism Mitochondria Autophagy Neuroprotection CaMkk β/AMPK pathway |
| 基金项目:广西卫生厅立项项目（Z2016220）；广西中医药大学2018年广西一流学科建设项目重点课题（2018XK089） |
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| 中文摘要: |
| 目的：观察敛肝熄风止颤方对帕金森病（Parkinson Disease，PD）的影响，探讨其神经保护机制。方法：将60只SD大鼠分为假手术组10只，造模组50只，造模组大鼠接受PD模型制备，将成模的40只大鼠随机分为模型组10只、低剂量组（0.36 g/kg）10只、中剂量组（0.72 g/kg）及高剂量组（1.44 g/kg）10只，持续灌胃给药30 d，比较各组大鼠阿扑吗啡诱导旋转次数、圆筒实验，纹状体超微结构以及CaMkkβ、AMPK、p-AMPK水平的变化。结果：1）敛肝熄风止颤方可明显减少大鼠转圈以及肢体碰壁的次数，随着剂量增加次数减少更明显，差异有统计学意义(P<0.05)。2）造模大鼠纹状体线粒体自噬现象减弱，敛肝熄风止颤方可明显促进脑组织线粒体自噬。3）中药干预后大鼠纹状体CaMkkβ、p-AMPK蛋白表达上调，与模型组比较，差异有统计学意义（P<0.05），其中高剂量组较低剂量组上调明显，差异有统计学意义（P<0.05）。结论：敛肝熄风止颤方对帕金森病具有神经保护作用，其机制之一可能是通过激活CaMkk/AMPK通路活性促进线粒体自噬有关。 |
| English Summary: |
| To observe the effect of Lianggan Xifeng Zhichan Formula (LGXFZC) on Parkinson's disease (Parkinson's disease,PD) and explore its neuroprotective mechanism.Methods:A total of 60 SD rats were divided into a sham operation group (n=10) and a model group (n=50).The rats in the model group were made by PD model.40 rats were randomly divided into a model group (n=10),a low dose group (0.36 g/kg) (n=10),a middle dose group (0.72 g/kg) and a high dose group (1.44 g/kg) for 30 days.The rotation times of apomorphine,cylinder test,ultrastructure of striatum and the levels of CaMkk β,AMPK and p-AMPK were compared in each group.Results:1) LGXFZC could significantly reduce the frequency of rotation and limb touching wall in rats.As the dose increases,the frequency decreases more obviously.The difference was statistically significant (P<0.05).2) the phenomenon of mitochondrial autophagy in striatum of model rats was weakened,and LGXFZC could obviously promote mitochondrial autophagy in brain tissue.3) after the intervention of Chinese medicine,the expression of CaMkk β and p-AMPK protein in the striatum of rats was significantly higher than that in the model group (P<0.05),and compared with the model group,the difference is statistically significant (P<0.05).Among them,the high-dose group and the lower-dose group were up-regulated significantly (P<0.05).Conclusion:LGXFZC has neuroprotective effect,and one of its mechanisms may be that it promotes mitochondrial autophagy by activating the activity of CaMkk/AMPK pathway. |
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