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艾灸通过下调NR2B表达对大鼠脑缺血/再灌注损伤的神经保护作用

Neuroprotective Effect of Moxibustion on Cerebral Ischemia/Reperfusion Injury in Rats by Downregulating NR2B Expression.

作者信息

Di Zhong, Guo Qin, Zhang Quanai

机构信息

Department of Acupuncture and Moxibustion, The Third Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China.

Department of Acupuncture and Moxibustion, The Third School of Clinical Medicine, Zhejiang Chinese Medical University, Hangzhou, China.

出版信息

Evid Based Complement Alternat Med. 2021 Oct 25;2021:5370214. doi: 10.1155/2021/5370214. eCollection 2021.

DOI:10.1155/2021/5370214
PMID:34733340
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8560262/
Abstract

OBJECTIVE

Stroke is a common and frequently occurring disease of the central nervous system, which is characterized by high mortality and a high disability rate. Moxibustion is a common method for treating stroke in traditional Chinese medicine, but its neuroprotective mechanism is unknown. N-Methyl-D-Aspartate Receptor Subunit 2B (NR2B) plays an important role in neuronal apoptosis. The objective of this study was to explore the mechanisms underlying the neuroprotective effect of moxibustion on cerebral ischemia/reperfusion (I/R) injury based on NR2B.

METHODS

Sprague-Dawley rats were randomly divided into 5 groups: the control group, I/R group, I/R + moxibustion group, I/R + Ro25-6981 (NR2B antagonist) group, and I/R + Ro25-6981 + moxibustion group. The cerebral ischemia/reperfusion model was induced by middle cerebral artery occlusion. Before the establishment of the model, the Ro25-6981 group received intraperitoneal injections of Ro25-6981, the moxibustion group received moxibustion, and the Ro25-6981 + moxibustion group received both interventions. The neurological dysfunction was evaluated by a neurological deficiency score (NDS). The infarct volume was examined by TTC (2,3,5-triphenyltetrazolium chloride) staining. The apoptosis rate of cerebral cells in the ischemic area was examined by TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling) staining, and the expression of Bcl-2, Bax, and caspase-3 was observed by western blot. NR2B and JNK were also observed by western blot.

RESULTS

Compared with the I/R group, moxibustion significantly decreased the neurological deficiency score ( < 0.05) and the infarct rate ( < 0.01) in I/R rats which were similar to those in the Ro25-6981 group. After moxibustion treatment, there was a significant decrease in the apoptosis rate ( < 0.001) and the protein expression levels of Bax, caspase-3, and JNK ( < 0.001) and an increase in the expression of Bcl-2 ( < 0.01). Compared with the I/R group, moxibustion downregulated the expression of NR2B and decreased the activity of NR2B in the cerebral ischemia area ( < 0.001).

CONCLUSIONS

Moxibustion can improve neurological dysfunction and decrease infarction area and neuronal apoptosis caused by cerebral ischemia/reperfusion in rats. Its neuroprotective mechanism may be related to downregulating the expression of NR2B.

摘要

目的

中风是中枢神经系统常见且多发的疾病,具有高死亡率和高致残率的特点。艾灸是中医治疗中风的常用方法,但其神经保护机制尚不清楚。N-甲基-D-天冬氨酸受体亚基2B(NR2B)在神经元凋亡中起重要作用。本研究旨在探讨基于NR2B的艾灸对脑缺血/再灌注(I/R)损伤神经保护作用的机制。

方法

将Sprague-Dawley大鼠随机分为5组:对照组、I/R组、I/R+艾灸组、I/R+Ro25-6981(NR2B拮抗剂)组和I/R+Ro25-6981+艾灸组。采用大脑中动脉闭塞法诱导脑缺血/再灌注模型。在模型建立前,Ro25-6981组腹腔注射Ro25-6981,艾灸组进行艾灸,Ro25-6981+艾灸组接受两种干预。通过神经功能缺损评分(NDS)评估神经功能障碍。采用2,3,5-氯化三苯基四氮唑(TTC)染色检测梗死体积。采用末端脱氧核苷酸转移酶介导的dUTP缺口末端标记(TUNEL)染色检测缺血区脑细胞凋亡率,通过蛋白质免疫印迹法观察Bcl-2、Bax和半胱天冬酶-3的表达。还通过蛋白质免疫印迹法观察NR2B和JNK。

结果

与I/R组相比,艾灸显著降低了I/R大鼠的神经功能缺损评分(<0.05)和梗死率(<0.01),与Ro25-6981组相似。艾灸治疗后,凋亡率(<0.001)、Bax、半胱天冬酶-3和JNK的蛋白表达水平显著降低(<0.001),Bcl-2表达增加(<0.01)。与I/R组相比,艾灸下调了脑缺血区NR2B的表达并降低了NR2B的活性(<0.001)。

结论

艾灸可改善大鼠脑缺血/再灌注所致的神经功能障碍,减少梗死面积和神经元凋亡。其神经保护机制可能与下调NR2B的表达有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b11/8560262/a785ef2f6114/ECAM2021-5370214.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b11/8560262/7b0658e035f3/ECAM2021-5370214.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b11/8560262/c61046c48aaf/ECAM2021-5370214.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b11/8560262/7ed2e2975163/ECAM2021-5370214.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b11/8560262/96da2a8b7b2a/ECAM2021-5370214.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b11/8560262/0cf74a7a25ea/ECAM2021-5370214.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b11/8560262/a785ef2f6114/ECAM2021-5370214.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b11/8560262/7b0658e035f3/ECAM2021-5370214.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b11/8560262/c61046c48aaf/ECAM2021-5370214.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b11/8560262/7ed2e2975163/ECAM2021-5370214.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b11/8560262/96da2a8b7b2a/ECAM2021-5370214.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b11/8560262/0cf74a7a25ea/ECAM2021-5370214.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b11/8560262/a785ef2f6114/ECAM2021-5370214.006.jpg

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