Electroacupuncture at GV20-GB7 regulates mitophagy to protect against neurological deficits following intracerebral hemorrhage via inhibition of apoptosis

被引：17

作者：

Guan, Ruiqiao ^{[1
,2
,3
,4
,5
,6
]}

Li, Zhihao ^{[7
]}

Dai, Xiaohong ^{[2
,3
]}

Zou, Wei ^{[2
,3
]}

Yu, Xueping ^{[2
,3
]}

Liu, Hao ^{[8
]}

Chen, Qiuxin ^{[2
,3
,4
]}

Teng, Wei ^{[2
,3
]}

Liu, Peng ^{[2
,3
]}

Liu, Xiaoying ^{[2
,3
]}

Dong, Shanshan ^{[2
,3
,4
]}

机构：

[1] Fudan Univ, Zhongshan Hosp, Dept Integrated Chinese & Western Med, Shanghai 200032, Peoples R China

[2] Heilongjiang Univ Chinese Med, Dept Clin Med, Harbin 150040, Heilongjiang, Peoples R China

[3] Heilongjiang Univ Chinese Med, Affiliated Hosp 1, Dept Acupuncture & Moxibust 3, 26 Heping Rd, Harbin 150040, Heilongjiang, Peoples R China

[4] Heilongjiang Univ Chinese Med, Clin Key Lab Integrated Chinese & Western Med, Harbin 150040, Heilongjiang, Peoples R China

[5] London South Bank Univ, Dept Tradit Chinese Med, London SE1 6RD, England

[6] London Confucius Inst Tradit Chinese Med, Clin Tradit Chinese Med, London SE1 0AA, England

[7] Shanghai Univ Chinese Med, Yueyang Hosp Integrated Tradit Chinese & Western, Dept Acupuncture & Moxibust, Shanghai 200437, Peoples R China

[8] Tongdc Hosp Zhejiang Prov, Dept Acupuncture & Moxibust, Hangzhou 315099, Zhejiang, Peoples R China

来源：

MOLECULAR MEDICINE REPORTS | 2021年 / 24卷 / 01期

基金：

中国国家自然科学基金; 黑龙江省自然科学基金; 国家教育部博士点专项基金资助;

关键词：

intracerebral hemorrhage; electroacupuncture; autophagy; mitophagy; apoptosis; CEREBRAL ISCHEMIC-INJURY; TRAUMATIC BRAIN-INJURY; BCL-2; FAMILY-MEMBERS; CELL-DEATH; SUBARACHNOID HEMORRHAGE; SCALP ACUPUNCTURE; RAT MODEL; MITOCHONDRIAL DYSFUNCTION; AUTOPHAGY ACTIVATION; MEDIATED MITOPHAGY;

D O I：

10.3892/mmr.2021.12131

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The acupuncture penetrating line of Baihui (GV20) to Qubin (GB7) spans the parietal, frontal and temporal lobes. The present study aimed to elucidate the mechanism by which electroacupuncture (EA) at GV20-GB7 regulates mitophagy in intracerebral hemorrhage (ICH) and whether it serves a neuroprotective role. A whole blood-induced ICH model was used. Mitophagy-regulating proteins, including BCL/adenovirus E1B 19 kDa-interacting protein 3 (BNIP3), PTEN-induced putative kinase 1 (PINK1), Parkin and apoptosis-associated proteins were detected by western blotting; autophagy following ICH was evaluated by immunofluorescent techniques; morphological characteristics of mitophagy were observed using transmission electron microscopy; and TUNEL assay was performed to determine the number of apoptotic cells. Immunohistochemistry was used to detect p53 expression. The protective role of EA (GV20-GB7) via enhanced mitophagy and suppressed apoptosis in ICH was further confirmed by decreased modified neurological severity score. The results showed that EA (GV20-GB7) treatment upregulated mitochondrial autophagy following ICH and inhibited apoptotic cell death. The mechanism underlying EA (GV20-GB7) treatment may involve inhibition of p53, an overlapping protein of autophagy and apoptosis. EA (GV20-GB7) treatment decreased neurobehavioral deficits following ICH but pretreatment with 3-methyladenine counteracted the beneficial effects of EA (GV20-GB7) treatment. In conclusion, EA (GV20-GB7) improved recovery from ICH by regulating the balance between mitophagy and apoptosis.

引用

页数：15

共 1 条

[1] Recombinant Osteopontin Improves Neurological Functional Recovery and Protects Against Apoptosis via PI3K/Akt/GSK-3β Pathway Following Intracerebral Hemorrhage
Zhang, Wenqian
Cui, Ying
Gao, Junling
Li, Ran
Jiang, Xiaohua
Tian, Yanxia
Wang, Kaijie
Cui, Jianzhong
MEDICAL SCIENCE MONITOR, 2018, 24 : 1588 - 1596

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