Mechanisms Involved in the Neuroprotection of Electroacupuncture Therapy for Ischemic Stroke

Xing, Ying; Zhang, Min; Li, Wenbin; Dong, Fang; Zhang, Feng

doi:10.3389/fnins.2018.00929

Cited by 57 publications

(54 citation statements)

References 100 publications

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“…Cannabinoid receptors are expressed in brain tissue, and activation of these receptors give rise to neuroprotection against brain IRI. In our previous studies, we found that activation of the CB1 cannabinoid receptor by ACEA decreased brain IRI by restoring mitochondrial functions, and inhibition of mitochondrial permeability transition pore (MPTP) opening may be involved in the neuroprotective effects of ACEA 3,25 . Since the opening of the MPTP and subsequent mitochondrial swelling and enlargement lead to mitochondrial fission, we hypothesized that ACEA protects neuronal function in brain IRI by regulating mitochondrial fission.…”

Section: Discussionmentioning

confidence: 99%

“…The cells were plated into a 24-well cell culture plate. After the treatments, the supernatant of each well was collected, and the LDH activity in the supernatant was determined by using an LDH reagent kit as previously described 3 .…”

Section: Cell Viability and Ldh Release Assaysmentioning

confidence: 99%

“…The in vitro and in vivo protein levels were evaluated by using the Bradford method. Western blot procedures were performed as previously described 3 . We used the following primary antibodies: anti-cleaved caspase-3, anti-Drp1, anti-Fis1, anti-Mff, anti-CB1, and anti-β-actin (1:200 in dilution).…”

Section: Western Blot Analysismentioning

confidence: 99%

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Cannabinoid CB1 receptor agonist ACEA alleviates brain ischemia/reperfusion injury via CB1–Drp1 pathway

Yang

Wang

et al. 2020

Cell Death Discov.

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Activation of the cannabinoid CB1 receptor induces neuroprotection against brain ischemia/reperfusion injury (IRI); however, the mechanism is still unknown. In this study, we used oxygen-glucose deprivation/reoxygenation (OGD/R)-induced injury in neuronal cells and middle cerebral artery occlusion (MCAO)-induced brain IRI in rats to mimic ischemic brain injury, and hypothesized that the CB1 receptor agonist arachidonyl-2-chloroethylamide (ACEA) would protect ischemic neurons by inhibiting mitochondrial fission via dynamin-related protein 1 (Drp1). We found that OGD/R injury reduced cell viability and mitochondrial function, increased lactate dehydrogenase (LDH) release, and increased cell apoptosis, and mitochondrial fission. Notably, ACEA significantly abolished the OGD/R-induced neuronal injuries described above. Similarly, ACEA significantly reversed MCAO-induced increases in brain infarct volume, neuronal apoptosis and mitochondrial fission, leading to the recovery of neurological functions. The neuroprotective effects of ACEA were obviously blocked by coadministration of the CB1 receptor antagonist AM251 or by the upregulation of Drp1 expression, indicating that ACEA alleviates brain IRI via the CB1–Drp1 pathway. Our findings suggest that the CB1 receptor links aberrant mitochondrial fission to brain IRI, providing a new therapeutic target for brain IRI treatment.

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Section: Discussionmentioning

confidence: 99%

Section: Cell Viability and Ldh Release Assaysmentioning

confidence: 99%

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Cannabinoid CB1 receptor agonist ACEA alleviates brain ischemia/reperfusion injury via CB1–Drp1 pathway

Yang

Wang

et al. 2020

Cell Death Discov.

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“…According to our previous studies, EA can improve neurological dysfunction, decrease the infarct volumes, and decrease the number of ischemic lesions (Xing et al, 2018a,b). Moreover, EA treatment could generate neuro regenerative effects for ischemic stroke, including promoting brain blood flow, regulating oxidative stress, reducing excitatory amino acids with neurotoxicity, maintaining the integrity of the blood-brain barrier, inhibiting neuronal apoptosis, increasing neurotrophic factors and producing brain ischemic tolerance (Xing et al, 2018c). Therefore, early intervention with EA in the acute stage of ischemic stroke has very important clinical significance.…”

Section: Introductionmentioning

confidence: 99%

Electroacupuncture Inhibits Neuronal Autophagy and Apoptosis via the PI3K/AKT Pathway Following Ischemic Stroke

Wang

Zhang

Feng

et al. 2020

Front. Cell. Neurosci.

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Electroacupuncture (EA) is a safe and effective therapy for ischemic stroke in both clinical and laboratory settings. However, the underlying mechanism behind EA treatment for stroke remains unclear. Here, we aimed to evaluate whether EA treatment at the acupoints of Zusanli (ST36) and Quchi (LI11) exerted a neuroprotective effect on ischemic stroke rats by modulating autophagy and apoptosis via the PI3K/AKT/mTOR signaling pathway. EA was performed at 24 h following brain ischemia/reperfusion (I/R) for 30 min per day for 3 days. Our results indicated that EA treatment significantly decreased neurological deficits and cerebral infarct volume in ischemic stroke rats. Also, EA intervention markedly reduced neuronal apoptosis by suppressing the activation of cleaved caspase-3 (CCAS3) at 72 h following I/R, as shown by a Western blot analysis. Furthermore, EA treatment after ischemic stroke suppressed the ischemia activated expression level of LC3II/I and Atg7 and increased the ischemia inhibited expression level of PI3K, phosphorylation of mTOR, phosphorylation of AKT, P62 and LAMP1, hence mediating the autophagy level of the neurocyte, which was reversed by the PI3K inhibitor Dactolisib. In summary, our results indicate that the protective effects of EA treatment at points of Quchi (LI11) and Zusanli (ST36) in rats following cerebral I/R injury was associated with the inhibition of neuronal apoptosis and autophagy via activating the PI3K/AKT/mTOR signaling pathway.

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“…Acupuncture helps harmonize Yin and Yang, then clearing blocked channels of Qi and Blood in the body so as to restore the normal body state, thus reducing motor impairment. A number of previous clinical trials have demonstrated the efficacy of acupuncture as a post-stroke intervention [9][10][11].…”

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confidence: 99%

Efficacy and Mechanism of Abdominal Acupuncture as a Poststroke Intervention for Promoting Upper-limb Motor Recovery: A Study Protocol of A Randomized Controlled Trial

Pan

Ling

Xie

et al. 2019

Preprint

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Background: How to promote true recovery from poststroke upper limb motor impairment has remained an urgent public health problem. Acupuncture has the potential to facilitate poststroke recovery. Abdominal acupuncture, based on the recently discovered acupoint system on the anterior abdominal wall, appears attractive because it induces less pain, and allows concurrent limb rehabilitative training during treatment. However, its clinical efficacy has not been systematically demonstrated, and its neurophysiological mechanism has remained obscure. Methods: First-onset stroke survivors (0.5-3 months post-stroke) will be randomly divided into 3 groups (N=22 in each), respectively receiving (1) abdominal acupuncture, (2) abdominal acupuncture with sham needles, and (3) no acupuncture. All subjects will concurrently receive basic treatment, including upper limb rehabilitative training and measures for secondary stroke prevention. Clinical scores reflective of motor functions and impairment (Wolf motor function test, Fugl-Meyer assessment, Brunnstrom staging), evaluation of daily life ability, surface electromyography, and motor-imagery functional magnetic resonance imaging will be collected as outcome measures before and after intervention. Upper-limb muscle synergies will be identified from the collected surface electromyography. Discussion: The study will use abdominal acupuncture to improve recovery from motor dysfunction of the upper limb after stroke, to observe the effects of abdominal acupuncture on post-stroke upper limb motor functions, and to analyze the relationship between changes in upper-limb functions and measurements from both multi-muscle surface electromyographic data and brain activations during motor imagery from functional magnetic resonance imaging, so as to explore possible mechanisms of neuroplasticity associated with abdominal acupuncture. Trial registration: This trial was registered with the ClinicalTrials.gov (ID: NCT03712085) on 7th July 2018, and last updated on 16th Oct 2018.

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Mechanisms Involved in the Neuroprotection of Electroacupuncture Therapy for Ischemic Stroke

Cited by 57 publications

References 100 publications

Cannabinoid CB1 receptor agonist ACEA alleviates brain ischemia/reperfusion injury via CB1–Drp1 pathway

Cannabinoid CB1 receptor agonist ACEA alleviates brain ischemia/reperfusion injury via CB1–Drp1 pathway

Electroacupuncture Inhibits Neuronal Autophagy and Apoptosis via the PI3K/AKT Pathway Following Ischemic Stroke

Efficacy and Mechanism of Abdominal Acupuncture as a Poststroke Intervention for Promoting Upper-limb Motor Recovery: A Study Protocol of A Randomized Controlled Trial

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