title: Phosphatidylinositol 3-kinase/Akt signaling pathway mediates acupuncture-induced dopaminergic neuron protection and motor function improvement in a mouse model of Parkinson's disease.
abstract: It has been reported that acupuncture treatment reduced dopaminergic neuron degeneration in Parkinson's disease (PD) models. However, the mechanistic pathways underlying, such neuroprotection, are poorly understood. Here, we investigated the effects and the underlying mechanism of acupuncture in a mouse model of PD using 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). First, we observed that MPTP-induced impairment of Akt activation, but not MPTP-induced c-Jun activation, was effectively restored by acupuncture treatment in the substantia nigra. Furthermore, we demonstrated for the first time that the brain-specific blockade of phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway, by intranasal administration of LY294002, a specific inhibitor of PI3K/Akt signaling pathway, significantly blocked acupuncture-induced dopaminergic neuron protection and motor function improvement. Our results provide evidence that PI3K/Akt signaling pathway may play a central role in the mechanism underlying acupuncture-induced benefits in Parkinsonian mice.
authors.affiliation: Studies of Translational Acupuncture Research (STAR), Acupuncture & Meridian Science Research Center (AMSRC), Kyung Hee University, 1 Hoegi-dong, Dongdaemoon-gu, Seoul, Republic of Korea.
authors.forename: Seung-Nam
authors.initials: SN
authors.lastname: Kim
authors.forename: Seung-Tae
authors.initials: ST
authors.lastname: Kim
authors.forename: Ah-Reum
authors.initials: AR
authors.lastname: Doo
authors.forename: Ji-Yeun
authors.initials: JY
authors.lastname: Park
authors.forename: Woongjoon
authors.initials: W
authors.lastname: Moon
authors.forename: Younbyoung
authors.initials: Y
authors.lastname: Chae
authors.forename: Chang Shik
authors.initials: CS
authors.lastname: Yin
authors.forename: Hyejung
authors.initials: H
authors.lastname: Lee
authors.forename: Hi-Joon
authors.initials: HJ
authors.lastname: Park
mesh_terms: D026881:Acupuncture; D015669:Acupuncture Points; D000281:Administration, Intranasal; D000818:Animals; D002867:Chromones / Q000008:administration & dosage; D004195:Disease Models, Animal; D059290:Dopaminergic Neurons / Q000187:drug effects / Q000502:physiology*; D004791:Enzyme Inhibitors / Q000008:administration & dosage; D005786:Gene Expression Regulation / Q000187:drug effects / Q000502:physiology; D020267:MPTP Poisoning / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009025:Morpholines / Q000008:administration & dosage; D009043:Motor Activity / Q000187:drug effects / Q000502:physiology*; D019869:Phosphatidylinositol 3-Kinases; D016755:Proto-Oncogene Proteins c-jun / Q000378:metabolism; D045442:Rotarod Performance Test; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology*; D013378:Substantia Nigra / Q000166:cytology* / Q000187:drug effects; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
chemical_list: D002867:Chromones; D004791:Enzyme Inhibitors; D009025:Morpholines; D016755:Proto-Oncogene Proteins c-jun; C085911:2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; D014446:Tyrosine 3-Monooxygenase; D019869:Phosphatidylinositol 3-Kinases