Abstract
BackgroundDuring 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.MethodsIschemia-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.ResultsEA 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.ConclusionAstroglial 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.
Highlights
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
The modified neurological severity scores (mNSS) scores were ameliorated in the middle cerebral artery occlusion and reperfusion (MCAO/R) + EA group at Days 3 and 7 after EA treatment, as compared with the MCAO/R group (Day3: P = 0.044, Day7: P = 0.027, Fig. 1b) and the MCAO/R+ Non-EA group (Day3: P = 0.031, Day7: P = 0.032, Fig. 1b), These results demonstrated that EA could produce neuroprotective effects against neurological and motor deficits induced by MCAO/R
GFAP-positive cells of the MCAO/R + EA group were lower than the MCAO/R group (CA1: P = 0.001, cortex: P = 0.023, Fig. 4d) and the MCAO/R+ Non-EA group (CA1: P < 0.001, cortex: P = 0.001, Fig. 4c) at Day 7 after EA. These results suggested that EA treatment could inhibit astroglial and microglial/macrophage hyperplasia in peri-infarct hippocampal CA1 and sensorimotor of MCAO/R rats
Summary
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. EA for the role of purine receptors in the central nervous system has not yet been reported. Electroacupuncture (EA) is an effective and safe strategy used for anti-inflammation and anti-nociception of many diseases [1,2,3]. EA acts on purine receptors in the central nervous system(CNS) has not yet been reported. It is well-documented that extracellular ATP triggers surrounding glial purinergic receptors signaling pathway and pro-inflammatory cytokines release to aggravate neural injury in cerebral ischemia [8, 9]. We speculate that purinergic receptors might play dualistic roles in response to EA effects treating inflammatory injury induced by ischemia
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