title: Electroacupuncture protects against ischemic stroke by reducing autophagosome formation and inhibiting autophagy through the mTORC1-ULK1 complex-Beclin1 pathway.
abstract: 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.
authors.affiliation: College of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, P.R. China.
authors.forename: Weilin
authors.initials: W
authors.lastname: Liu
authors.affiliation: The Fujian Province Key Laboratory of Motor Functional Rehabilitation, Fuzhou, Fujian 350001, P.R. China.
authors.forename: Guanhao
authors.initials: G
authors.lastname: Shang
authors.affiliation: Rehabilitation Hospital Affiliated to Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350001, P.R. China.
authors.forename: Shanli
authors.initials: S
authors.lastname: Yang
authors.affiliation: College of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, P.R. China.
authors.forename: Jia
authors.initials: J
authors.lastname: Huang
authors.affiliation: Rehabilitation Hospital Affiliated to Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350001, P.R. China.
authors.forename: Xiehua
authors.initials: X
authors.lastname: Xue
authors.affiliation: The Fujian Province Key Laboratory of Motor Functional Rehabilitation, Fuzhou, Fujian 350001, P.R. China.
authors.forename: Yunjiao
authors.initials: Y
authors.lastname: Lin
authors.affiliation: The Fujian Province Key Laboratory of Motor Functional Rehabilitation, Fuzhou, Fujian 350001, P.R. China.
authors.forename: Yi
authors.initials: Y
authors.lastname: Zheng
authors.affiliation: The Fujian Province Key Laboratory of Motor Functional Rehabilitation, Fuzhou, Fujian 350001, P.R. China.
authors.forename: Xian
authors.initials: X
authors.lastname: Wang
authors.affiliation: The Fujian Province Key Laboratory of Motor Functional Rehabilitation, Fuzhou, Fujian 350001, P.R. China.
authors.forename: Lulu
authors.initials: L
authors.lastname: Wang
authors.affiliation: The Fujian Province Key Laboratory of Motor Functional Rehabilitation, Fuzhou, Fujian 350001, P.R. China.
authors.forename: Ruhui
authors.initials: R
authors.lastname: Lin
authors.affiliation: College of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, P.R. China.
authors.forename: Jing
authors.initials: J
authors.lastname: Tao
authors.affiliation: College of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, P.R. China.
authors.forename: Lidian
authors.initials: L
authors.lastname: Chen
mesh_terms: D015669:Acupuncture Points; D000818:Animals; D051017:Apoptosis Regulatory Proteins / Q000235:genetics / Q000378:metabolism*; D001343:Autophagy / Q000235:genetics; D000071189:Autophagy-Related Protein-1 Homolog; D000071186:Beclin-1; D004195:Disease Models, Animal; D015671:Electroacupuncture / Q000379:methods*; D006801:Humans; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics* / Q000378:metabolism; D008247:Lysosomes / Q000235:genetics / Q000378:metabolism; D000076222:Mechanistic Target of Rapamycin Complex 1; D046912:Multiprotein Complexes / Q000235:genetics / Q000378:metabolism; D018696:Neuroprotective Agents; D010588:Phagosomes / Q000235:genetics / Q000378:metabolism; D051381:Rats; D015427:Reperfusion Injury / Q000235:genetics / Q000473:pathology / Q000628:therapy*; D015398:Signal Transduction / Q000235:genetics; D020521:Stroke / Q000235:genetics / Q000473:pathology / Q000628:therapy*; D058570:TOR Serine-Threonine Kinases / Q000235:genetics / Q000378:metabolism
chemical_list: D051017:Apoptosis Regulatory Proteins; D000071186:Beclin-1; C512829:Becn1 protein, rat; D047908:Intracellular Signaling Peptides and Proteins; D046912:Multiprotein Complexes; D018696:Neuroprotective Agents; D000071189:Autophagy-Related Protein-1 Homolog; D000076222:Mechanistic Target of Rapamycin Complex 1; D058570:TOR Serine-Threonine Kinases; C586255:ULK1 protein, rat