世界中医药
文章摘要
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):.  
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)
作者单位
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 1 广西中医药大学药学院南宁530001 2 广西中医药大学附属瑞康医院神经内科南宁530011 
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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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