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BMC Complement Altern Med. 2017 Oct 10;17(1):480. doi: 10.1186/s12906-017-1974-y.

Electroacupuncture ameliorating post-stroke cognitive impairments via inhibition of peri-infarct astroglial and microglial/macrophage P2 purinoceptors-mediated neuroinflammation and hyperplasia.

Author information

1
College of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian, 350122, China.
2
Fujian Key Laboratory of Rehabilitation Technology, Fuzhou, Fujian, 350122, China.
3
College of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian, 350122, China. taojing01@163.com.
4
College of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian, 350122, China. fjtcm1958@sina.com.

Abstract

BACKGROUND:

During ischemic stroke (IS), adenosine 5'-triphosphate (ATP) is released from damaged nerve cells of the infract core region to the extracellular space, invoking peri-infarct glial cellular P2 purinoceptors singling, and causing pro-inflammatory cytokine secretion, which is likely to initiate or aggravate motor and cognitive impairment. It has been proved that electroacupuncture (EA) is an effective and safe strategy used in anti-inflammation. However, EA for the role of purine receptors in the central nervous system has not yet been reported.

METHODS:

Ischemia-reperfusion injured rat model was induced by middle cerebral artery occlusion and reperfusion (MCAO/R). EA treatment at the DU 20 and DU 24 acupoints treatment were conducted to rats from the 12 h after MCAO/R injury for consecutive 7 days. The neurological outcomes, infarction volumes and the level of astroglial and microglial/macrophage hyperplasia, inflammatory cytokine and P2X7R and P2Y1R expression in the peri-infarct hippocampal CA1and sensorimotor cortex were investigated after IS to evaluate the MCAO/R model and therapeutic mechanism of EA treatment.

RESULTS:

EA effectively reduced the level of pro-inflammatory cytokine interleukin-1β (IL-1β) as evidenced by reduction in astroglial and microglial/macrophage hyperplasia and the levels of P2X7R and ED1, P2X7R and GFAP, P2Y1R and ED1, P2Y1R and GFAP co-expression in peri-infarct hippocampal CA1 and sensorimotor cortex compared with that of MCAO/R model and Non-EA treatment, accompanied by the improved neurological deficit and the motor and memory impairment outcomes. Therefore, our data support the hypothesis that EA could exert its anti-inflammatory effect via inhibiting the astroglial and microglial/macrophage P2 purinoceptors (P2X7R and P2Y1R)-mediated neuroinflammation after MCAO/R injury.

CONCLUSION:

Astroglial and microglial/macrophage P2 purinoceptors-mediated neuroinflammation and hyperplasia in peri-infarct hippocampal CA1 and sensorimotor cortex were attenuated by EA treatment after ischemic stroke accompanied by the improved motor and memory behavior performance.

KEYWORDS:

Electroacupuncture; Glia; Ischemic stroke; Neuroinflammation; P2 purinoceptors

PMID:
29017492
PMCID:
PMC5635586
DOI:
10.1186/s12906-017-1974-y
[Indexed for MEDLINE]
Free PMC Article

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