2021
DOI: 10.3389/fnagi.2021.680706
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Electroacupuncture Pretreatment Prevents Cognitive Impairment Induced by Cerebral Ischemia–Reperfusion via Adenosine A1 Receptors in Rats

Abstract: A previous study has demonstrated that pretreatment with electroacupuncture (EA) induces rapid tolerance to focal cerebral ischemia. In the present study, we investigated whether adenosine receptor 1 (A1 R) is involved in EA pretreatment-induced cognitive impairment after focal cerebral ischemia in rats. Two hours after EA pretreatment, focal cerebral ischemia was induced by middle cerebral artery occlusion for 120 min in male Sprague-Dawley rats. The neurobehavioral score, cognitive function [as determined by… Show more

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Cited by 16 publications
(5 citation statements)
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“…Electrical stimulation of Zusanli may cause increased cerebral blood flow in normal rats or those with ischemic stroke and can enhance the functional connection between the ipsilateral motor cortex and motor function-related brain areas (including the motor cortex, striatum, and sensory cortex) in focal ischemic rats [ 23 , 24 ]. Furthermore, EA preconditioning can reduce the injury after cerebral ischemia-reperfusion and induce cerebral ischemic tolerance, and other effects have been confirmed [ 25 , 26 ]. Therefore, we hypothesize that EA preconditioning can reduce the inflammatory response during cerebral ischemia-reperfusion and reduce the iron overload caused by oxidative stress.…”
Section: Introductionmentioning
confidence: 99%
“…Electrical stimulation of Zusanli may cause increased cerebral blood flow in normal rats or those with ischemic stroke and can enhance the functional connection between the ipsilateral motor cortex and motor function-related brain areas (including the motor cortex, striatum, and sensory cortex) in focal ischemic rats [ 23 , 24 ]. Furthermore, EA preconditioning can reduce the injury after cerebral ischemia-reperfusion and induce cerebral ischemic tolerance, and other effects have been confirmed [ 25 , 26 ]. Therefore, we hypothesize that EA preconditioning can reduce the inflammatory response during cerebral ischemia-reperfusion and reduce the iron overload caused by oxidative stress.…”
Section: Introductionmentioning
confidence: 99%
“…α7nAchR is a target of a cholinergic anti-inflammatory signalling pathway that is widely expressed on the surface of alveolar epithelial and immune cells and is activated primarily by the release of acetylcholine from vagal efferent nerves ( 44 ). Previous studies have demonstrated that EA treatment can exhibit potent organ protective effects in various disease conditions, such as postoperative ileus ( 8 ), doxorubicin-induced cardiotoxicity ( 45 ), cerebral IR injury ( 46 ), and hepatic IR injury ( 47 ), and this protective role of EA stimulation is mostly dependent on the activation of α7nAchR. It is worth noting that the therapeutic effects of EA therapy on a variety of organs are directly related to multiple signalling pathways mediated by α7nAchR, in which the α7nAchR-mediated Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3(STAT3) signalling pathway ( 48 ), high-mobility group Box 1(HMGB1)/nuclear factor-κB (NF-κB) signalling pathway ( 49 ), and NLRP3 signalling pathway ( 18 ) have been regarded as significantly associated with the organ-protective effects of EA treatment.…”
Section: Discussionmentioning
confidence: 99%
“…Inhibition of A1R specifically was shown to cause cochlear nerve damage and to increase susceptibility to HL ( Vlajkovic et al, 2017 ). However, intracranially, A1R has a neuroprotective effect ( Shi et al, 2021 ), and disruption of A1R exacerbates long-term potentiation of the hippocampus, which can cause CI ( Zhang et al, 2020 ). A2R represents a class of adenosine receptors that have been extensively studied and found to be associated with pathophysiological conditions such as inflammatory diseases and neurodegenerative disorders.…”
Section: Co-morbidity Hypothesismentioning
confidence: 99%