Acupuncture inhibits microglial activation and inflammatory events in the MPTP-induced mouse model.
Using a mouse model of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinson's disease (PD), this study investigated on the neuroprotective effects of acupuncture by examining whether acupuncture contributed to inhibiting microglial activation and inflammatory events. C57BL/6 mice were treated with MPTP (30 mg/kg, i.p.) for 5 consecutive days. Acupuncture was then applied to acupoints Yanglingquan (GB34) and Taichong (LR3) starting 2 h after the first MPTP administration and then at 48 h intervals until the mice were sacrificed for analyses at 1, 3, and 7 days after the last MPTP injection. These experiments demonstrated that acupuncture inhibited the decreased of the tyrosine hydroxylase (TH) immunoreactivity (IR) and generated a neuroprotective effects in the striatum (ST) and the substantia nigra (SN) on days 1, 3, and 7 post-MPTP injections. Acupuncture attenuated the increase of macrophage antigen complex-1 (MAC-1), a marker of microglial activation, at 1 and 3 days and reduced the increases in cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) expression on days 1, 3, and 7. In MPTP group, striatal dopamine (DA) was measured by 46% at 7 days, whereas DA in the acupuncture group was 78%. On the basis of these results, we suggest that acupuncture could be used as a neuroprotective intervention for the purpose of inhibiting microglial activation and inflammatory events in PD.
Kang
Jun Mo
JM
Department of Meridian and Acupoints, College of Korean Medicine, Kyung Hee University, Seoul, South Korea; WHO Collaborating Centre for Traditional Medicine, East-West Medical Research Institute, Kyung Hee University, Seoul, South Korea.
Park
Hi Joon
HJ
Choi
Yeong Gon
YG
Choe
Il Hwan
IH
Park
Jae Hyun
JH
Kim
Yong Sik
YS
Lim
Sabina
S
D026881:Acupuncture / Q000379:methods* / Q000639:trends; D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D003342:Corpus Striatum / Q000378:metabolism / Q000503:physiopathology; D051546:Cyclooxygenase 2 / Q000378:metabolism; D019610:Cytoprotection / Q000502:physiology*; D004195:Disease Models, Animal; D004298:Dopamine / Q000096:biosynthesis; D004660:Encephalitis / Q000139:chemically induced / Q000517:prevention & control / Q000628:therapy*; D005911:Gliosis / Q000139:chemically induced / Q000517:prevention & control / Q000628:therapy*; D016177:Macrophage-1 Antigen / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D017628:Microglia / Q000187:drug effects / Q000502:physiology*; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D020734:Parkinsonian Disorders / Q000503:physiopathology / Q000517:prevention & control / Q000628:therapy*; D013378:Substantia Nigra / Q000378:metabolism / Q000503:physiopathology; D016896:Treatment Outcome; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism; D015854:Up-Regulation / Q000502:physiology
D015415:Biomarkers; D016177:Macrophage-1 Antigen; D052247:Nitric Oxide Synthase Type II; D014446:Tyrosine 3-Monooxygenase; D051546:Cyclooxygenase 2; C489691:Ptgs2 protein, rat; D004298:Dopamine