Electroacupuncture protects against ischemic stroke by reducing autophagosome formation and inhibiting autophagy through the mTORC1-ULK1 complex-Beclin1 pathway

被引：123

作者：

Liu, Weilin ^{[1
]}

Shang, Guanhao ^{[2
]}

Yang, Shanli ^{[3
]}

Huang, Jia ^{[1
]}

Xue, Xiehua ^{[3
]}

Lin, Yunjiao ^{[2
]}

Zheng, Yi ^{[2
]}

Wang, Xian ^{[2
]}

Wang, Lulu ^{[2
]}

Lin, Ruhui ^{[2
]}

Tao, Jing ^{[1
]}

Chen, Lidian ^{[1
]}

机构：

[1] Fujian Univ Tradit Chinese Med, Coll Rehabil Med, 1 Qiuyang Rd, Fuzhou 350122, Fujian, Peoples R China

[2] Fujian Univ Tradit Chinese Med, Fujian Prov Key Lab Motor Funct Rehabilitat, Fuzhou 350001, Fujian, Peoples R China

[3] Fujian Univ Tradit Chinese Med, Rehabilitat Hosp, Fuzhou 350001, Fujian, Peoples R China

来源：

INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE | 2016年 / 37卷 / 02期

基金：

中国国家自然科学基金;

关键词：

electroacupuncture; autophagy; mammalian target of rapamycin complex 1; Unc-51-like kinase complex; Beclin1; FOCAL CEREBRAL-ISCHEMIA; QUANTITATIVE GAIT ANALYSIS; CELL-DEATH; UP-REGULATION; INJURED RATS; BRAIN-INJURY; ACTIVATION; REPERFUSION; BECLIN-1; ACUPUNCTURE;

D O I：

10.3892/ijmm.2015.2425

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

100103 [病原生物学]; 100218 [急诊医学];

摘要：

In a previous study by our group, we demonstrated that electroacupuncture (EA) activates the class I phosphoinositide 3-kinase (PI3K)/Akt signaling pathway. There is considerable evidence that the downstream mammalian target of rapamycin complex 1 (mTORC1) plays an important role in autophagy following ischemic stroke. The aim of the present study was to determine whether EA exerts a neuroprotective effect through mTORC1-mediated autophagy following ischemia/reperfusion injury. Our results revealed that EA at the LI11 and ST36 acupoints attenuated motor dysfunction, improved neurological deficit outcomes and decreased the infarct volumes. The number of autophagosomes, autolysosomes and lysosomes was decreased following treatment with EA. Simultaneously, the levels of the autophagosome membrane maker, microtubule-associated protein 1 light chain 3 beta (LC3B)II/I, Unc-51-like kinase 1 (ULK1), autophagy related gene 13 Atg13) and Beclin1 (ser14) were decreased, whereas mTORC1 expression was increased in the peri-infarct cortex. These results suggest that EA protects against ischemic stroke through the inhibition of autophagosome formation and autophagy, which is mediated through the mTORC1-ULK complex-Beclin1 pathway.

引用

页码：309 / 318

页数：10

共 70 条

[1]

Buckley Kathleen M, 2014, Exp Transl Stroke Med, V6, P8, DOI 10.1186/2040-7378-6-8

[2]

Electroacupuncture at the Quchi and Zusanli acupoints exerts neuroprotective role in cerebral ischemia-reperfusion injured rats via activation of the PI3K/Akt pathway [J].