Electroacupuncture protects the brain against acute ischemic injury via up-regulation of delta-opioid receptor in rats

Tian, Xue; Fei, Zhou; Yang, Ru; Xia, Ying; Wu, Guosheng; Guo, Jing

doi:10.3736/jcim20080617

Cited by 32 publications

(23 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Unfortunately, although studies revealed that multiple EA improves neurological function in animal stroke models [14], there is less experimental evidence upon the underlying mechanisms of multiple EA treatment. Previous studies showed that multiple EA induces expression of Ang-1 and Ang-2 [15] and δ -opioid receptor [9] as well. However, whether multiple EA stimulation induces changes similar to those upon single-time EA stimulation?…”

Section: Introductionmentioning

confidence: 99%

Neurotrophic Signaling Factors in Brain Ischemia/Reperfusion Rats: Differential Modulation Pattern between Single‐Time and Multiple Electroacupuncture Stimulation

Wang

Yang

Liu

et al. 2014

Evidence-Based Complementary and Alternative Medicine

View full text Add to dashboard Cite

Electroacupuncture (EA) treatment has been widely used for stroke-like disorders in traditional Chinese medicine. However, the underlying mechanisms remain unclear. Our previous studies showed that single-time EA stimulation at “Baihui” (GV 20) and “Shuigou” (GV 26) after the onset of ischemia can protect the brain against ischemic injury in rats with middle cerebral artery occlusion (MCAO). Here, we further investigated the differential effects between multiple EA and single-time EA stimulation on ischemic injury. In the present study, we found that both single-time EA and multiple EA stimulation significantly reduced MCAO-induced ischemic infarction, while only multiple EA attenuated sensorimotor dysfunctions. Also, with PCR array screening and ingenuity gene analysis, we revealed that multiple EA and single-time EA stimulation could differentially induce expression changes in neurotrophic signaling related genes. Meanwhile, with western blotting, we demonstrated that the level of glia maturation factor β (GMFβ) increased in the early stage (day 1) of reperfusion, and this upregulation was suppressed only by single-time EA stimulation. These findings suggest that the short-term effect of single-time EA stimulation differs from the cumulative effect of multiple EA, which possibly depends on their differential modulation on neurotrophic signaling molecules expression.

show abstract

Section: Introductionmentioning

confidence: 99%

Neurotrophic Signaling Factors in Brain Ischemia/Reperfusion Rats: Differential Modulation Pattern between Single‐Time and Multiple Electroacupuncture Stimulation

Wang

Yang

Liu

et al. 2014

Evidence-Based Complementary and Alternative Medicine

View full text Add to dashboard Cite

show abstract

“…DOR activation with DADLE also increases the tolerance of cultured cortical neurons against hypoxia [10]. Furthermore, we showed that DOR provides neuroprotection against hypoxic/ischemic insults in various models including neurons under hypoxia, brain slices in hypoxia or oxygen-glucose deprivation and in vivo brain exposed to cerebral ischemia [12,13,14,15,16,17,18,19,20,21,22,23]. Intracerebroventricular treatment with the DOR agonist TAN-67 (60 nmol) significantly reduced the infarct volume and attenuated neurological deficits, while Naltrindole, a DOR antagonist, aggravated ischemic damage after forebrain ischemia in rats [12].…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2013

View full text Add to dashboard Cite

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

show abstract

“…Electroacupuncture can also upregulate DOR expression in the ischemic brain and thus protect the brain from ischemic injury [15] that can cause epilepsy secondary to cerebral infarction [74]. Most interestingly, direct subacute high-frequency electrical stimulation of the parahippocampal cortex in patients with intractable medial temporal lobe epilepsy also produces an antiepileptic effect, which is associated with reduced opioid peptide binding including 3 H-DAMGO, 3 H-DPDPE, and 3 H-nociceptin (the ligand for MOR, DOR, and a fourth opioid, nociception receptor, resp.)…”

Section: Potential Mechanisms Of Acupuncture Inhibition Of Neuronamentioning

confidence: 99%

“…Some acupuncture-induced effects involve the activation of the opioid system [8–13]. We have previously demonstrated that electroacupuncture has a neuroprotective role in the brain against ischemic injury via the δ -opioid system [14, 15]. DOR expression/activation inhibits Na + channel activity [16, 17] and thus attenuates Na + -K + homeostasis of the cortex under normoxic/hypoxic conditions [16, 18–22].…”

Section: Introductionmentioning

confidence: 99%

From Acupuncture to Interaction betweenδ-Opioid Receptors and Na⁺Channels: A Potential Pathway to Inhibit Epileptic Hyperexcitability

Chao

Shen

Xia

2013

Evidence-Based Complementary and Alternative Medicine

View full text Add to dashboard Cite

Epilepsy is one of the most common neurological disorders affecting about 1% of population. Although the precise mechanism of its pathophysiological changes in the brain is unknown, epilepsy has been recognized as a disorder of brain excitability characterized by recurrent unprovoked seizures that result from the abnormal, excessive, and synchronous activity of clusters of nerve cells in the brain. Currently available therapies, including medical, surgical, and other strategies, such as ketogenic diet and vagus nerve stimulation, are symptomatic with their own limitations and complications. Seeking new strategies to cure this serious disorder still poses a big challenge to the field of medicine. Our recent studies suggest that acupuncture may exert its antiepileptic effects by normalizing the disrupted neuronal and network excitability through several mechanisms, including lowering the overexcited neuronal activity, enhancing the inhibitory system, and attenuating the excitatory system in the brain via regulation of the interaction between δ-opioid receptors (DOR) and Na+ channels. This paper reviews the progress in this field and summarizes new knowledge based on our work and those of others.

show abstract

Electroacupuncture protects the brain against acute ischemic injury via up-regulation of delta-opioid receptor in rats

Abstract: EA can up-regulate DOR expression and protect the brain from ischemia-reperfusion injury.

Cited by 32 publications

References 16 publications

Neurotrophic Signaling Factors in Brain Ischemia/Reperfusion Rats: Differential Modulation Pattern between Single‐Time and Multiple Electroacupuncture Stimulation

Neurotrophic Signaling Factors in Brain Ischemia/Reperfusion Rats: Differential Modulation Pattern between Single‐Time and Multiple Electroacupuncture Stimulation

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

From Acupuncture to Interaction betweenδ-Opioid Receptors and Na⁺Channels: A Potential Pathway to Inhibit Epileptic Hyperexcitability

Contact Info

Product

Resources

About

Electroacupuncture protects the brain against acute ischemic injury via up-regulation of delta-opioid receptor in rats

Abstract: EA can up-regulate DOR expression and protect the brain from ischemia-reperfusion injury.

Cited by 32 publications

References 16 publications

Neurotrophic Signaling Factors in Brain Ischemia/Reperfusion Rats: Differential Modulation Pattern between Single‐Time and Multiple Electroacupuncture Stimulation

Neurotrophic Signaling Factors in Brain Ischemia/Reperfusion Rats: Differential Modulation Pattern between Single‐Time and Multiple Electroacupuncture Stimulation

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

From Acupuncture to Interaction betweenδ-Opioid Receptors and Na+Channels: A Potential Pathway to Inhibit Epileptic Hyperexcitability

Contact Info

Product

Resources

About

From Acupuncture to Interaction betweenδ-Opioid Receptors and Na⁺Channels: A Potential Pathway to Inhibit Epileptic Hyperexcitability