Electroacupuncture and Brain Protection against Cerebral Ischemia: Specific Effects of Acupoints

Fei, Zhou; Guo, J.; Cheng, Jin-Wei; Wu, Gen-Cheng; Sun, Jian; Xia, Ying

doi:10.1155/2013/804397

Cited by 21 publications

(35 citation statements)

References 18 publications

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“…Although the primary cause of ischemic infarction is insufficient blood supply to the brain region involved and an increase in the blood flow can greatly relieve the ischemic infarction [45,46,47], this work demonstrated that DOR protection against brain ischemia does not rely on the regulation of cerebral blood flow because either DOR activation or inhibition had no appreciable effect on cerebral blood flow in non-ischemic and ischemic conditions. It is very likely that DOR exerts its protection through other mechanisms, especially the molecules for membrane and intercellular signaling.…”

Section: Discussionmentioning

confidence: 96%

δ-Opioid Receptor Activation Rescues the Functional TrkB Receptor and Protects the Brain from Ischemia-Reperfusion Injury in the Rat

et al. 2013

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Objectivesδ-opioid receptor (DOR) activation reduced brain ischemic infarction and attenuated neurological deficits, while DOR inhibition aggravated the ischemic damage. The underlying mechanisms are, however, not well understood yet. In this work, we asked if DOR activation protects the brain against ischemic injury through a brain-derived neurotrophic factor (BDNF) -TrkB pathway.MethodsWe exposed adult male Sprague-Dawley rats to focal cerebral ischemia, which was induced by middle cerebral artery occlusion (MCAO). DOR agonist TAN-67 (60 nmol), antagonist Naltrindole (100 nmol) or artificial cerebral spinal fluid was injected into the lateral cerebroventricle 30 min before MCAO. Besides the detection of ischemic injury, the expression of BDNF, full-length and truncated TrkB, total CREB, p-CREB, p-ATF and CD11b was detected by Western blot and fluorescence immunostaining.ResultsDOR activation with TAN-67 significantly reduced the ischemic volume and largely reversed the decrease in full-length TrkB protein expression in the ischemic cortex and striatum without any appreciable change in cerebral blood flow, while the DOR antagonist Naltrindole aggregated the ischemic injury. However, the level of BDNF remained unchanged in the cortex, striatum and hippocampus at 24 hours after MCAO and did not change in response to DOR activation or inhibition. MCAO decreased both total CREB and pCREB in the striatum, but not in the cortex, while DOR inhibition promoted a further decrease in total and phosphorylated CREB in the striatum and decreased pATF-1 expression in the cortex. In addition, MCAO increased C11b expression in the cortex, striatum and hippocampus, and DOR activation specifically attenuated the ischemic increase in the cortex but not in the striatum and hippocampus.ConclusionsDOR activation rescues TrkB signaling by reversing ischemia/reperfusion induced decrease in the full-length TrkB receptor and reduces brain injury in ischemia/reperfusion

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Section: Discussionmentioning

confidence: 96%

δ-Opioid Receptor Activation Rescues the Functional TrkB Receptor and Protects the Brain from Ischemia-Reperfusion Injury in the Rat

et al. 2013

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“…The effect on the blood flow is greatly dependent on the location stimulated, the stimulation intensity and frequency, and the duration of EA (Zhou et al , 2011b; Zhou et al , 2013a; Zhou et al , 2013b). Interestingly, the increase in blood flow occurred only in the ischemic, but not in the non-ischemic, brain (Zhou et al , 2011b).…”

Section: Acupuncturementioning

confidence: 99%

Non-pharmaceutical therapies for stroke: Mechanisms and clinical implications

Chen

Luo

et al. 2014

Progress in Neurobiology

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Stroke is deemed a worldwide leading cause of neurological disability and death, however, there is currently no promising pharmacotherapy for acute ischemic stroke aside from intravenous or intra-arterial thrombolysis. Yet because of the narrow therapeutic time window involved, thrombolytic application is very restricted in clinical settings. Accumulating data suggest that non-pharmaceutical therapies for stroke might provide new opportunities for stroke treatment. Here we review recent research progress in the mechanisms and clinical implications of non-pharmaceutical therapies, mainly including neuroprotective approaches such as hypothermia, ischemic/hypoxic conditioning, acupuncture, medical gases, transcranial laser therapy, etc. In addition, we briefly summarize mechanical endovascular recanalization devices and recovery devices for the treatment of the chronic phase of stroke and discuss the relative merits of these devices.

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“…A decrease in sympathetic tone may result from a similar pathway as presented in Figure 2.3, in which vasodilation occurs from the release of CGRP [68,114]. Changes in activity of different brain regions in response to EA may also be responsible for the decrease in SNS activity, e.g.…”

Section: Electroacupuncturementioning

confidence: 92%

“…However, much is still to be learned about how this stimulation actually causes hemodynamic changes. Moreover, the results from multiple studies involving neurostimulation and its effects on blood flow are conflicting [32,36,[63][64][65][66][67][68]. To date, there is no real consensus on which neurostimulation technique offers the best treatment, mainly because the parameters used differ widely throughout the literature and most studies have not focused on direct comparisons for different disease states.…”

Section: Overview and Aims Of The Thesismentioning

confidence: 99%

“…However, EA use is limited by the need for a licensed acupuncturist to properly place the electrodes at the correct acupoints. In addition, most of the research involving EA has been conducted on animals, and with mixed results [64,68,113,155]. For the pilot study, we compared our results to other healthy, human subject studies using similar protocols with TENS.…”

Section: Justification For the Use Of Tensmentioning

confidence: 99%

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Investigating Hemodynamic Responses to Electrical Neurostimulation

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Investigating Hemodynamic Responses to Electrical Neurostimulation Sean YouraSince the 1900s, the number of deaths attributable to cardiovascular disease has steadily risen. With the advent of antihypertensive drugs and non-invasive surgical procedures, such as intravascular stenting, these numbers have begun to level off. Despite this trend, the number of patients diagnosed with some form of cardiovascular disease has only increased. By 2030, prevalence of coronary heart disease is expected to increase approximately by 18% in the United States. By 2050, prevalence of peripheral arterial occlusive disease is expected to increase approximately by 98% in the U.S. No single drug or surgical intervention offers a complete solution to these problems. Thus, a multifaceted regimen of lifestyle changes, medication, and device or surgical interventions is usually necessary. A potential adjunct therapy and cost-effective solution for treating cardiovascular disease that has been overlooked is neurostimulation.Recent studies show that using neurostimulation techniques, such as transcutaneous electrical nerve stimulation (TENS), can help to reduce ischemic pain, lower blood pressure, increase blood flow to the periphery, and decrease systemic vascular resistance. The mechanisms by which these hemodynamic changes occur is still under investigation. The primary aim of this thesis is to elucidate these mechanisms through a thorough synthesis of the existing literature on this subject. Neurostimulation, specifically TENS, is thought to modulate both the metaboreflex and norepinephrine release from sympathetic nerve terminals.To test the hypothesis that TENS increases local blood flow, decreases mean arterial pressure, and decreases cutaneous vascular resistance compared to placebo, in which the electrodes are attached but no electrical stimulation is applied, a protocol was developed to test the effect of neurostimulation on healthy subjects. Implementation of this protocol in a pilot study will determine if neurostimulation causes significant changes in blood flow using the most relevant perfusion measurement instrumentation. Before conducting this study, pre-pilot comparison studies of interferential current therapy (IFC) versus TENS, low frequency (4 Hz) TENS versus high frequency (100 Hz) TENS, and electrode placement on the back versus the forearm were conducted. The only statistically significant difference found was that the application of IFC on the back decreased the reperfusion time, meaning that the time required to reach the average baseline perfusion unit value after occlusion decreased. Further pre-pilot work investigating these different modalities and parameters is necessary to ensure that favorable hemodynamic changes can be detected in the pilot study.

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Electroacupuncture and Brain Protection against Cerebral Ischemia: Specific Effects of Acupoints

Cited by 21 publications

References 18 publications

δ-Opioid Receptor Activation Rescues the Functional TrkB Receptor and Protects the Brain from Ischemia-Reperfusion Injury in the Rat

δ-Opioid Receptor Activation Rescues the Functional TrkB Receptor and Protects the Brain from Ischemia-Reperfusion Injury in the Rat

Non-pharmaceutical therapies for stroke: Mechanisms and clinical implications

Investigating Hemodynamic Responses to Electrical Neurostimulation

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