Electroacupuncture attenuated cerebral ischemic injury and neuroinflammation through α7nAChR-mediated inhibition of NLRP3 inflammasome in stroke rats

Jiang, Tao; Wu, Mingyan; Zhang, Zhanqin; Yan, Chaoying; Ma, Zhi; He, Shan; Yuan, Wei; Pu, Kairui; Wang, Qiang

doi:10.1186/s10020-019-0091-4

Cited by 68 publications

(54 citation statements)

References 45 publications

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“…Hippocampal NF-κB mRNA expression, and serum TNF-α and IL-1β levels were increased in response to ischemia stroke ( 8 ). Cerebral ischemia-reperfusion injury activated the NLRP3 inflammasome proteins in rats, which could be suppressed by electroacupuncture, leading to improvement of neurological deficit scores and infarct sizes in middle cerebral artery occlusion (MCAO) model rats ( 9 ).…”

Section: Introductionmentioning

confidence: 99%

Carthamin yellow improves cerebral ischemia‑reperfusion injury by attenuating inflammation and ferroptosis in rats

et al. 2021

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Carthamin yellow (CY), a flavonoid compound extracted from safflower, has been reported to attenuate cardiac ischemia and reperfusion injury. However, whether CY could ameliorate ischemic stroke is not completely understood. In the present study, the preventive effects of CY on experimental ischemic stroke were investigated using middle cerebral artery occlusion (MCAO) model rats. Neurological scores, brain edema, infarct area and microtubule-associated protein 2 (MAP-2) immunoreactivity were assessed to evaluate the effects of CY on ischemic brain injury. The involvement of inflammation and ferroptosis were examined to investigate the mechanism underlying the effects of CY. The results demonstrated that 2-week CY treatment attenuated the neurological deficit score, brain water content and infarct area, and increased MAP-2 immunoreactivity in the cortex in MCAO model rats. CY administration also deactivated the cortex NF-κB/NLR family pyrin domain containing 3 inflammasome signaling pathway, and decreased serum TNF-α, IL-1β and IL-6 concentrations. Moreover, CY treatment inhibited Fe 2+ and reactive oxygen species accumulation, and reversed acyl-CoA synthetase long-chain family member 4, transferrin receptor 1, glutathione peroxidase 4 and ferritin heavy chain 1 protein expression levels in the brain. The levels of glutathione, superoxide dismutase and malondialdehyde in the serum were also reversed by CY treatment. Collectively, the results of the present study demonstrated that CY protected rats against ischemic stroke, which was associated with mitigation of inflammation and ferroptosis.

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Section: Introductionmentioning

confidence: 99%

Carthamin yellow improves cerebral ischemia‑reperfusion injury by attenuating inflammation and ferroptosis in rats

et al. 2021

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“…Using the PPI-T test, we performed the first pharmacological experiments on the effects of nicotinic receptor (nAChRs) agonists α7 and α4β2 subtypes (respectively PNU-282987 (PNU) and RJR2403) on HBH, in low selective doses equal to their K i and some higher. It is known that nAChRs are involved in hypoxic or ischaemic preconditioning in the brain and other organs, and it was most convincingly demonstrated for the α7 and α4β2nAChRs [ 40 , 41 , 42 , 43 , 44 ]. In our experiments, PNU (but not RJR2403), and more pronouncedly its solvent dimethyl sulfoxide (DMSO, 2–3%), showed a PPI-associated effect on the efficiency of HBH, the direction of which changed to the opposite at the border when PPI = 36–40% [ 20 , 45 ].…”

Section: Introductionmentioning

confidence: 99%

Opposite Pathways of Cholinergic Mechanisms of Hypoxic Preconditioning in the Hippocampus: Participation of Nicotinic α7 Receptors and Their Association with the Baseline Level of Startle Prepulse Inhibition

et al. 2020

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(1) Background. A one-time moderate hypobaric hypoxia (HBH) has a preconditioning effect whose neuronal mechanisms are not studied well. Previously, we found a stable correlation between the HBH efficiency and acoustic startle prepulse inhibition (PPI). This makes it possible to predict the individual efficiency of HBH in animals and to study its potential adaptive mechanisms. We revealed a bi-directional action of nicotinic α7 receptor agonist PNU-282987 and its solvent dimethyl sulfoxide on HBH efficiency with the level of PPI > or < 40%. (2) The aim of the present study was to estimate cholinergic mechanisms of HBH effects in different brain regions. (3) Methods: in rats pretested for PPI, we evaluated the activity of synaptic membrane-bound and water-soluble choline acetyltransferase (ChAT) in the sub-fractions of ‘light’ and ‘heavy’ synaptosomes of the neocortex, hippocampus and caudal brainstem in the intact brain and after HBH. We tested the dose-dependent influence of PNU-282987 on the HBH efficiency. (4) Results: PPI level and ChAT activity correlated negatively in all brain structures of the intact animals, so that the values of the latter were higher in rats with PPI < 40% compared to those with PPI > 40%. After HBH, this ChAT activity difference was leveled in the neocortex and caudal brainstem, while for membrane-bound ChAT in the ‘light’ synaptosomal fraction of hippocampus, it was reversed to the opposite. In addition, a pharmacological study revealed that PNU-282987 in all used doses and its solvent displayed corresponding opposite effects on HBH efficiency in rats with different levels of PPI. (5) Conclusion: We substantiate that in rats with low and high PPI two opposite hippocampal cholinergic mechanisms are involved in hypoxic preconditioning, and both are implemented by forebrain projections via nicotinic α7 receptors. Possible causes of association between general protective adaptation, HBH, PPI, forebrain cholinergic system and hippocampus are discussed.

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“…EA at Shuigou (GV26) significantly improved the neurological deficit symptoms in rats with ischemic stroke, which may be involved in upregulating Wnt7a and LEF1 proteins and mRNAs levels and decreasing GSK-3 β and DKK1 proteins and mRNAs levels [ 37 ]. Jiang et al showed a novel anti-inflammatory mechanism induced by EA via α 7nAChR-mediated inhibition of NLRP3 inflammasome in rats after cerebral ischemic injury [ 38 ].…”

Section: The Therapeutic Effect Of Ea For Ischemic Stroke In Expermentioning

confidence: 99%

The Therapeutic Effect of Electroacupuncture Therapy for Ischemic Stroke

Xing

Zhang

2020

Evidence-Based Complementary and Alternative Medicine

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Electroacupuncture (EA) stimulation is a supplementary therapy and commonly applied in treatment of ischemic stroke in clinic. Stroke is an important cause of long-term disability in individuals in both developing and developed countries. In our review, we show the application of EA stimulation for apoplectic pain, limbs spasticity, blood flow interruption, depression, swallowing dysfunction, aphasia, urinary incontinence, cognition and memory impairment, and constipation following stroke in patients and the related mechanisms in animals. The effectiveness of EA involves with acupoints, intensity, intervals, and duration of intervention for treatment of stroke. The combination of EA and common rehabilitation treatment may exert better effect compared with EA alone. In summary, EA might provide a potential treatment strategy for treating apoplectic patients in clinic.

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Electroacupuncture attenuated cerebral ischemic injury and neuroinflammation through α7nAChR-mediated inhibition of NLRP3 inflammasome in stroke rats

Cited by 68 publications

References 45 publications

Carthamin yellow improves cerebral ischemia‑reperfusion injury by attenuating inflammation and ferroptosis in rats

Carthamin yellow improves cerebral ischemia‑reperfusion injury by attenuating inflammation and ferroptosis in rats

Opposite Pathways of Cholinergic Mechanisms of Hypoxic Preconditioning in the Hippocampus: Participation of Nicotinic α7 Receptors and Their Association with the Baseline Level of Startle Prepulse Inhibition

The Therapeutic Effect of Electroacupuncture Therapy for Ischemic Stroke

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