Effects of electroacupuncture preconditioning on activity of dynamin-related protein 1 in brain tissues during cerebral ischemia-reperfusion in rats
10.3760/cma.j.issn.0254-1416.2017.12.023
- VernacularTitle:电针预处理对大鼠脑缺血再灌注时脑组织动力相关蛋白1活性的影响
- Author:
Zhaoliang ZHANG
1
;
Yuqiu LIU
;
Gaofeng ZHANG
;
Fei SHI
;
Huailong CHEN
;
Zeng YIN
;
Fei XIAO
;
Mingshan WANG
Author Information
1. 261053,潍坊医学院麻醉学系
- Keywords:
Electric stimulation therapy;
Ischemic preconditioning;
Reperfusion injury;
Brain;
Dynamins;
Mitochondria
- From:
Chinese Journal of Anesthesiology
2017;37(12):1498-1501
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the effect of electroacupuncture (EA) preconditioning on the activity of dynamin-related protein 1 (Drp1) in brain tissues during cerebral ischemia-reperfusion (I/R) in rats.Methods A total of 126 pathogen-free healthy adult male Wistar rats,weighing 250-300 g,were divided into 3 groups (n =42 each) using a random number table:sham operation group (group S),group I/R and EA preconditioning group (group EA).In group S,the blood vessels were only separated but not occluded.In group I/R,a nylon thread with rounded tip was inserted into the left middle cerebral artery advanced cranially until resistance was met,and middle cerebral artery occlusion was maintained for 2 h followed by reperfusion.In group EA,Baihui acupoints were stimulated with an electric stimulator (2/ 15 Hz disperse-dense waves,intensity 1 mA) for 30 min,lasting for 5 consecutive days,and the model of focal cerebral I/R was established at 24 h after the last stimulation.At 6,24 and 48 h of reperfusion,the neurologic deficit was assessed and scored,the mitochondria in the cerebral cortex on the ischemic side were extracted,the expression of Drpl in mitochondria was detected using Western blot,the mitochondrial uhrastructure was examined with an electron microscope,and neuroapoptosis was measured using TUNEL.The apoptosis rate was calculated.Results Compared with group S,the neurological deficit score and apoptosis rate were significantly increased,and the expression of Drpl in mitochondria was up-regulated at each time point in I/R and EA groups (P＜0.05).Compared with group I/R,the neurological deficit score and apoptosis rate were significantly decreased,and the expression of Drpl in mitochondria was down-regulated at each time point in group EA (P＜0.05).Conclusion The mechanism by which EA preconditioning reduces cerebral I/R injury may be related to inhibiting the activity of Drpl and thus inhibiting the excessive fission of mitochondria in rats.
