Electroacupuncture upregulates Cezanne expression and alleviates focal cerebral ischemia/reperfusion inflammatory injury by inhibiting nuclear factor kappa B signal pathway in rats

Wenhao LU; Xueling ZHOU; Yikun REN; Jingwen WANG; Jun ZHU; Hongbei XU; Jiani LI; Yong LUO

doi:10.16016/j.1000-5404.202009102

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Electroacupuncture upregulates Cezanne expression and alleviates focal cerebral ischemia/reperfusion inflammatory injury by inhibiting nuclear factor kappa B signal pathway in rats

Basic Medicine | 更新时间：2026-01-09

- Electroacupuncture upregulates Cezanne expression and alleviates focal cerebral ischemia/reperfusion inflammatory injury by inhibiting nuclear factor kappa B signal pathway in rats
- Journal of Third Military Medical University Vol. 43, Issue 4, Pages: 283-294(2021)
- 作者机构：
  
  1.400016 重庆，重庆医科大学附属第一医院神经内科
  2.404010 重庆，重庆医科大学附属第二医院神经内科
- 作者简介：
- 基金信息：
  
  the General Program of National Natural Science Foundation of China(30470606);the National Natural Science Foundation for Young Scholar of China(81403243);the Project of Science and Technology Plan of Yuzhong District, Chongqing(20160102)
- DOI：10.16016/j.1000-5404.202009102
  CLC： R245.97;R363.21;R743.31
- Received：13 September 2020，
  
  Revised：2020-10-10，
  
  Published：15 April 2021
- 稿件说明：
移动端阅览
Wenhao LU, Xueling ZHOU, Yikun REN, et al. Electroacupuncture upregulates Cezanne expression and alleviates focal cerebral ischemia/reperfusion inflammatory injury by inhibiting nuclear factor kappa B signal pathway in rats[J]. Journal of Third Military Medical University, 2021, 43(4): 283-294.
DOI：

Wenhao LU, Xueling ZHOU, Yikun REN, et al. Electroacupuncture upregulates Cezanne expression and alleviates focal cerebral ischemia/reperfusion inflammatory injury by inhibiting nuclear factor kappa B signal pathway in rats[J]. Journal of Third Military Medical University, 2021, 43(4): 283-294. DOI： 10.16016/j.1000-5404.202009102.

摘要

目的

探讨电针上调Cezanne的表达及对局灶脑缺血/再灌注大鼠炎性损伤的神经保护作用。

方法

将SD大鼠按简单随机分组分为假手术（sham）组、电针（EA）组、缺血/再灌注（MCAO/R）组和缺血/再灌注+电针（MCAO/R+EA）组，颅内注射Cezanne沉默慢病毒（LV-shCezanne），空载慢病毒（vehicle）作为对照。采用改良线栓法制备右侧大脑中动脉缺血/再灌注模型，电针刺激“百会”穴和病侧“四关”穴（“合谷”/“太冲”穴）。缺血2 h后分别再灌注6、12、24、48、72 h和7 d。分别采用Garcia评分、TTC染色、Western blot、细胞计数，免疫荧光检测各组神经功能评分、梗死灶体积、缺血大脑皮质区Cezanne蛋白表达、Cezanne阳性细胞数、Cezanne的细胞分布类型、细胞核与细胞质NF-κB p65蛋白的表达。

结果

与sham组相比，EA组Cezanne蛋白表达在6 h和48 h增加(

0.05)，MCAO/R组Cezanne蛋白表达在12、24、48、72 h和7 d时增加（

0.05）；与MCAO/R组相比，MCAO/R+EA组Cezanne蛋白表达在12、24、72 h时进一步增加（

0.05）。相较于sham组，MCAO/R组神经评分降低（

0.05），Cezanne阳性细胞数、脑梗死体积增加（

0.05）；相较于MCAO/R组，MCAO/R+EA组神经评分升高（

0.05），Cezanne阳性细胞数增多（

0.05），脑梗死体积（

0.05）、p-IκBα/IκBα比值（

0.05）、细胞核p65/细胞质p65比值降低（

0.05）；免疫荧光显示Cezanne主要分布在缺血大脑皮质区神经元细胞质。

结论

电针通过上调Cezanne蛋白的表达，抑制大鼠局灶脑缺血/再灌注后NF-κB信号通路的激活，从而发挥神经保护作用。

Abstract

Objective

To investigate the roles of electroacupuncture (EA) in the upregulation of zinc finger protein Cezanne and in its neuroprotective effect on inflammatory injury induced by focal cerebral ischemia/reperfusion (I/R) in rats.

Methods

SD rats were randomized into sham group

EA group

I/R group and I/R+EA group. Cezanne silencing lentivirus (LV-shCezanne) was injection into the cerebral cortex to study the possible effect of Cezanne silencing on I/R injury

and injection of blank lentivirus (vehicle) as the control. The I/R model was established by conventional method of middle cerebral artery occlusion with ischemia for 2 h followed by reperfusion for 6

48 and 72 h and 7 d

respectively

and then EA was adopted to stimulate the Baihui acupoint and the Hegu and Taichong acupoints on the affected side. Garcia score

TTC staining

Western blotting

cell counting and immunofluorescence assay were performed in each group

so as to detect the neurological deficit score (NDS)

infarct size

Cezanne expression in the ischemic cerebral cortex

number and distribution of Cezanne positive cells

and expression of nuclear factor kappa B (NF- κB) p65 in the nucleus and cytoplasm.

Results

Compared with the sham group

the protein level of Cezanne was increased in EA group at 6 and 48 h (

0.05)

and also in the I/R group at 12

48 and 72 h (

0.05). While the level was further increased in the I/R+EA group at 12

72 and 7 d than the I/R group (

0.05). The NDS was significantly lower in the I/R group than the sham group (

0.05)

whereas the number of Cezanne positive cells and the size of cerebral infarct were obviously larger (

0.05). Compared with the I/R group

the I/R+EA group had higher NDS

more Cezanne positive cells

and smaller cerebral infarct size (

0.05)

and the ratios of both p-IκBα/IκBα and nucleus-p65 to cytoplasm-p65 were decreased in the MCAO/R+EA group (

0.05). Immunofluorescence assay showed that Cezanne was mainly distributed in the cytoplasm of neurons in ischemic cerebral cortex.

Conclusion

EA inhibits the activation of NF-κB signal pathway after focal cerebral I/R injury in rats by upregulating the expression of Cezanne protein

and then play a neuroprotective role in the process.

关键词

Keywords

references

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