Effect of electroacupuncture at “Shuigou” (GV26) and “Baihui” (GV20) on autophagy of hippo-campal neurons in rats with cerebral ischemia-reperfusion injury

LIU Dan-ni; ZHOU Jun; HUANG Xia-rong; SUN Guang-hua; LUO Fu; TAN Jin-qu; LIAO Yuan; PENG Ting; FENG Wei-bin

doi:10.13702/j.1000-0607.20210561

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Effect of electroacupuncture at “Shuigou” (GV26) and “Baihui” (GV20) on autophagy of hippo-campal neurons in rats with cerebral ischemia-reperfusion injury

更新时间：2023-08-11

- Effect of electroacupuncture at “Shuigou” (GV26) and “Baihui” (GV20) on autophagy of hippo-campal neurons in rats with cerebral ischemia-reperfusion injury
- Acupuncture Research Vol. 47, Issue 6, Pages: 491-496(2022)
- 作者机构：
  
  1. 南华大学附属第一医院康复医学中心
  2. 南华大学附属第一医院康复医学科
  3. 南华大学附属第一医院康复医学实验室
- 作者简介：
- 基金信息：
- DOI：10.13702/j.1000-0607.20210561
  CLC：
- Published：2022
- 稿件说明：
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LIU Dan-ni, ZHOU Jun, HUANG Xia-rong, et al. Effect of electroacupuncture at “Shuigou” (GV26) and “Baihui” (GV20) on autophagy of hippo-campal neurons in rats with cerebral ischemia-reperfusion injury[J]. Acupuncture research, 2022, 47(6): 491-496.
DOI：

LIU Dan-ni, ZHOU Jun, HUANG Xia-rong, et al. Effect of electroacupuncture at “Shuigou” (GV26) and “Baihui” (GV20) on autophagy of hippo-campal neurons in rats with cerebral ischemia-reperfusion injury[J]. Acupuncture research, 2022, 47(6): 491-496. DOI： 10.13702/j.1000-0607.20210561.

摘要

目的:探讨电针“水沟”“百会”穴对脑缺血再灌注(I/R)损伤大鼠海马神经元自噬的影响。方法:SD大鼠随机分为假手术组、模型组、电针组，每组16只。采用一侧大脑中动脉栓塞(MCAO)的方法复制I/R损伤大鼠模型。电针组予“水沟”“百会”电针治疗，20 min/次，1次/d

共5 d。以Longa神经功能评分法评价神经功能；TTC染色法测定大鼠脑梗死体积百分比；ELISA法检测脑脊液白细胞介素(IL)-6、IL-18、肿瘤坏死因子-α(TNF-α)含量；荧光定量PCR和Western blot法分别检测缺血区海马组织自噬相关蛋白腺苷酸活化蛋白激酶(AMPK)、Beclin-1、VPS34、LC3B mRNA和蛋白的表达。结果:与假手术组比较，模型组神经功能评分明显升高(P<0.01)

大鼠脑梗死体积百分比明显增大(P<0.01)

脑脊液IL-6、IL-18、TNF-α含量明显升高(P<0.01

P<0.05)

海马组织AMPK、Beclin-1、VPS34蛋白和mRNA表达水平，以及LC3B mRNA表达水平和LC3B-Ⅱ/LC3B-Ⅰ比值均升高(P<0.01

P<0.05)。与模型组比较，电针组神经功能评分降低(P<0.05)

脑梗死体积百分比缩小(P<0.05)

脑脊液IL-6、IL-18、TNF-α含量降低(P<0.05)

海马组织AMPK、Beclin-1、VPS34蛋白和mRNA表达水平，以及LC3B mRNA表达水平和LC3B-Ⅱ/LC3B-Ⅰ比值均降低(P<0.01

P<0.05)。结论:电针治疗可能通过抑制海马神经元自噬水平，缓解MCAO大鼠I/R损伤，减轻神经受损程度。

Abstract

Objective To explore the effect of electroacupuncture(EA) at “Shuigou”(GV6) and “Baihui”(GV20) on autophagy of hippocampal neurons in cerebral ischemia-reperfusion(I/R) injury rats. Methods Forty-eight healthy male SD rats were randomly divided into sham operation

model and EA groups

with 16 rats in each group. The rat model of cerebral I/R injury was established by occlusion of the middle cerebral artery(MCAO). Rats of the EA group received EA at GV26 and GV20 for 20 min

once daily for 5 days. The neurological function of rats in each group was evaluated by Longa neurological function score. The cerebral infarction volume was measured by TTC staining. The levels of IL-6

IL-18 and TNF-α in cerebrospinal fluid were detected by ELISA. Real-time PCR and Western blot were respectively used to detect the expressions of autophagy-related proteins AMPK

Beclin-1

VPS34 and LC3B. Results Compared with the sham operation group

neurological function scores of rats in the model group were significantly increased(P<0.01); the volume of cerebral infarction was significantly increased(P<0.01); the contents of IL-6

IL-18 and TNF-α in cerebrospinal fluid were increased(P<0.01

P<0.05); the mRNA expression levels of AMPK

Beclin-1

VPS34 and LC3B were significantly increased(P<0.01); the protein expressions of AMPK

Beclin-1

VPS34 and the ratio of LC3B-Ⅱ/LC3B-Ⅰ were increased(P<0.01

P<0.05). After intervention and in comparison with the model group

the neurological function scores were decreased(P<0.05); the cerebral infarct volume were decreased(P<0.05); the contents of IL-6

IL-18 and TNF-α in cerebrospinal fluid were decreased(P<0.05); the mRNA expressions of AMPK

Beclin-1

VPS34 and LC3B were significantly decreased(P<0.01); the protein expressions of AMPK

Beclin-1

VPS34 and the ratio of LC3 B-Ⅱ/LC3B-Ⅰ were decreased(P<0.05

P<0.01). Conclusion EA can improve the neurological function and alleviate the degree of nerve injury in rats with cerebral I/R injury

which may be related to inhibiting the autophagy level of hippocampal neurons.

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