Electroacupuncture promotes axonal regeneration in rats with focal cerebral ischemia through the downregulation of Nogo-A/NgR/RhoA/ROCK signaling

Huang, Simin; Huang, Danxia; Zhao, Jiapei; Chen, Lidian

doi:10.3892/etm.2017.4621

Cited by 14 publications

(11 citation statements)

References 38 publications

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“…GAP-43, as a key factor of axonal growth cones, participates in the process of axonal regeneration (Huang et al, 2017b). EA at acupoints of Neiguan and Zusanli may prompt neural remodeling and improve neural function in cerebral ischemic rats, which is related to promoted expression of GAP-43 surrounding the brain infarction region (Zhou et al, 2011).…”

Section: Literature Research Criteriamentioning

confidence: 99%

“…EA at acupoints of Neiguan and Zusanli may prompt neural remodeling and improve neural function in cerebral ischemic rats, which is related to promoted expression of GAP-43 surrounding the brain infarction region (Zhou et al, 2011). Nogo protein-A (Nogo-A) is a key myelin-related axonal growth inhibitory protein, mainly inhibiting axonal regeneration after ischemic stroke (Huang et al, 2017b). EA treatment at acupoints along both the Lung Meridian and the Pericardium Meridian may decrease the level of serum Nogo-A in post-stroke rats.…”

Section: Literature Research Criteriamentioning

confidence: 99%

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Mechanisms Involved in the Neuroprotection of Electroacupuncture Therapy for Ischemic Stroke

Xing

Zhang

et al. 2018

Front. Neurosci.

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Stroke is one of the main causes of death all over the world. As the combination of acupuncture and electric stimulation, electroacupuncutre is a safe and effective therapy, which is commonly applied in ischemic stroke therapy in both experimental studies and clinical settings. The review was performed via searching for related articles in the databases of OVID, PUBMED, and ISI Web of Science from their respective inceptions to May 2018. In this review, we summarized the mechanism of EA for ischemic stroke via a series of factors, consisting of apoptosis related-factors, inflammatory factors, autophagy-related factors, growth factors, transcriptional factors, cannabinoid CB1 receptors, and other factors. In summary, EA stimulation may effectively alleviate ischemic brain injury via a series of signal pathways and various other factors.

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Section: Literature Research Criteriamentioning

confidence: 99%

Section: Literature Research Criteriamentioning

confidence: 99%

Mechanisms Involved in the Neuroprotection of Electroacupuncture Therapy for Ischemic Stroke

Xing

Zhang

et al. 2018

Front. Neurosci.

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“…Thus, NgR might play a role in maintaining the stability of neuronal circuit and the plasticity of axon after cerebral ischaemia, especially in the late stage. Increased expression of NgR may be a compensatory response to cerebral ischaemia, playing an important role in the reconstruction of neuronal circuits and axon regeneration or remodelling . Moreover, our results showed that the expression of Nogo protein significantly increased in the early stage after CO intoxication, then gradually decreased at 1 month, and remained at a relatively constant level at 2 months after CO poisoning.…”

Section: Discussionmentioning

confidence: 50%

“…Increased expression of NgR may be a compensatory response to cerebral ischaemia, playing an important role in the reconstruction of neuronal circuits and axon regeneration or remodelling. [31][32][33] Moreover, our results showed that the expression of Nogo protein significantly increased in the early stage after CO intoxication, then gradually decreased at 1 month, and remained at a relatively constant level at 2 months after CO poisoning. This time-point coincided with the formation of extensive demyelination and delayed encephalopathy in rat brain tissue after CO poisoning, suggesting that the increased expression and activation of Nogo protein may be related to brain damage and the extensively demyelination following CO intoxication.…”

Section: Discussionmentioning

confidence: 51%

Fasudil alleviates brain damage in rats after carbon monoxide poisoning through regulating neurite outgrowth inhibitor/oligodendrocytemyelin glycoprotein signalling pathway

Wang

Guo

et al. 2019

Basic Clin Pharma Tox

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Carbon monoxide (CO) poisoning can lead to many serious neurological symptoms. Currently, there are no effective therapies for CO poisoning. In this study, rats exposed to CO received hyperbaric oxygen therapy, and those in the Fasudil group were given additional Fasudil injection once daily. We found that the escape latency in CO poisoning group (CO group) was significantly prolonged, the T1/Ttotal was obviously decreased, and the mean escape time and the active escape latency were notably extended compared with those in normal control group (NC group, P < 0.05). After administration of Fasudil, the escape latency was significantly shortened, T1/Ttotal was gradually increased as compared with CO group (>1 week, P < 0.05). Ultrastructural damage of neurons and blood‐brain barrier of rats was serious in CO group, while the structural and functional integrity of neuron and mitochondria maintained relatively well in Fasudil group. Moreover, we also noted that the expressions of neurite outgrowth inhibitor (Nogo), oligodendrocyte‐myelin glycoprotein (OMgp) and Rock in brain tissue were significantly increased in CO group, and the elevated levels of the three proteins were still observed at 2 months after CO poisoning. Fasudil markedly reduced their expressions compared with those of CO group (P < 0.05). In summary, the activation of Nogo‐OMgp/Rho signalling pathway is associated with brain injury in rats with CO poisoning. Fasudil can efficiently down‐regulate the expressions of Nogo, OMgp and Rock proteins, paving a way for the treatment of acute brain damage after CO poisoning.

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“…1 Among them, ischemic stroke accounts for about 87% of stroke cases. 2 In the acute phase of the disease, neurons of the ischemic lesion die quickly, while other neuron groups in the ischemic penumbra are vulnerable to secondary injury. 3 Unfortunately, despite advances in technology and pharmacology, there are still few drugs or treatments for stroke.…”

Section: Introductionmentioning

confidence: 99%

<p>Tanshinone IIA Promotes Axonal Regeneration in Rats with Focal Cerebral Ischemia Through the Inhibition of Nogo-A/NgR1/RhoA/ROCKII/MLC Signaling</p>

Wang¹,

Ni²,

Liu³

et al. 2020

DDDT

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The aim of this study was to evaluate the neuroprotective effect of tanshinone IIA (TSA) on focal cerebral ischemia in rats and to investigate whether it was associated with Nogo-A/NgR1/RhoA/Rho-associated protein kinase 2 (ROCKII)/myosin light chain (MLC) signaling. Methods: In this study, focal cerebral ischemia animal model was used. Neurological deficit scores and infarction volume were investigated to evaluate the neuroprotection of TSA. Hematoxylin-eosin staining, Nissl staining, and immunofluorescence staining were conducted to detect ischemic changes in brain tissue and changes in neurofilament protein 200 (NF200) and growth-associated protein-43 (GAP-43) expression, respectively. Western blotting and qRT-PCR analyses were used to detect the expression levels of NF200, GAP-43 and Nogo-A/NgR1/RhoA/ROCKII/MLC pathway-related signaling molecules. Results: TSA treatment can improve the survival rate of rats, reduce the neurological score and infarct volume, and reduce neuron damage. In addition, TSA also increased axon length and enhanced expression of NF200 and GAP-43. Importantly, TSA significantly attenuated the expression of Nogo-A, NgR1, RhoA, ROCKII, and p-MLC, and thus inhibiting the activation of this signaling pathway. Conclusion: TSA promoted axonal regeneration by inhibiting the Nogo-A/NgR1/RhoA/ ROCKII/MLC signaling pathway, thereby exerting neuroprotective effects in cerebral ischemia rats, which provided support for the clinical application of TSA in stroke treatment.

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Electroacupuncture promotes axonal regeneration in rats with focal cerebral ischemia through the downregulation of Nogo-A/NgR/RhoA/ROCK signaling

Cited by 14 publications

References 38 publications

Mechanisms Involved in the Neuroprotection of Electroacupuncture Therapy for Ischemic Stroke

Mechanisms Involved in the Neuroprotection of Electroacupuncture Therapy for Ischemic Stroke

Fasudil alleviates brain damage in rats after carbon monoxide poisoning through regulating neurite outgrowth inhibitor/oligodendrocytemyelin glycoprotein signalling pathway

<p>Tanshinone IIA Promotes Axonal Regeneration in Rats with Focal Cerebral Ischemia Through the Inhibition of Nogo-A/NgR1/RhoA/ROCKII/MLC Signaling</p>

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