Auricular vagus nerve stimulation promotes functional recovery and enhances the post-ischemic angiogenic response in an ischemia/reperfusion rat model

Jiang, Ying; Li, Longling; Ma, Jue; Zhang, Lina; Niu, Fei; Feng, Tao; Li, Changqing

doi:10.1016/j.neuint.2016.02.009

Cited by 50 publications

(45 citation statements)

References 43 publications

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“…Rats in the I/R group exhibited sustained neurobehavioral impairments as compared to the sham group in both tests, indicating that cerebral ischemia could induce neurological deficits. Ta-VNS treatment prevented neurological impairment, and these effects were also observed in the I/R+ta-VNS+LV-control group, which is consistent with our previous studies [11,12]. Nevertheless, the beneficial effects of ta-VNS were abrogated after PPAR-γ silencing (P < 0:05, Figures 2(d) and 2(e)).…”

Section: Inhibition Of Ppar-γ Weakens the Improvements Onsupporting

confidence: 90%

“…Transcutaneous electrical stimulation of the auricular branch of the vagus nerve (ta-VNS) has been proved to be an experimental therapeutic method to exert neuroprotective effects following cerebral ischemia. Our previous studies showed that ta-VNS treatment reduced infarct volume, promoted angiogenesis, and subsequent functional recovery in rat models of middle cerebral artery occlusion/reperfusion (MCAO/R) [11,12]. Most recently, it has been demonstrated that ta-VNS activated the vagal pathway and exerted neuroprotection similar to that of the traditional cervical vagus nerve stimulation (c-VNS) [13].…”

Section: Introductionmentioning

confidence: 99%

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PPAR-γ Mediates Ta-VNS-Induced Angiogenesis and Subsequent Functional Recovery after Experimental Stroke in Rats

Zhang

et al. 2020

BioMed Research International

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Background. Neoangiogenesis after cerebral ischemia in mammals is insufficient to restore neurological function, illustrating the need to design better strategies for improving outcomes. Our previous study has suggested that transcutaneous auricular vagus nerve stimulation (ta-VNS) induced angiogenesis and improved neurological functions in a rat model of cerebral ischemia/reperfusion (I/R) injury. However, the mechanisms involved need further exploration. Peroxisome proliferator-activated receptor-γ (PPAR-γ), well known as a ligand-modulated nuclear transcription factor, plays a crucial role in the regulation of cerebrovascular structure and function. Hence, the present study was designed to explore the role of PPAR-γ in ta-VNS-mediated angiogenesis and uncover the possible molecular mechanisms against ischemic stroke. Methods. Adult male Sprague–Dawley rats were transfected with either PPAR-γ small interfering RNA (siRNA) or lentiviral vector without siRNA prior to surgery and subsequently received ta-VNS treatment. The expression and localization of PPAR-γ in the ischemic boundary after ta-VNS treatment were examined. Subsequently, neurological deficit scores, neuronal damage, and infarct volume were all evaluated. Additionally, microvessel density, endothelial cell proliferation condition, and the expression of angiogenesis-related molecules in the peri-infarct cortex were measured. Results. We found that the expression of PPAR-γ in the peri-infarct cortex increased at 14 d and reached normal levels at 28 d after reperfusion. Ta-VNS treatment further upregulated PPAR-γ expression in the ischemic cortex. PPAR-γ was mainly expressed in neurons and astrocytes. Furthermore, ta-VNS-treated I/R rats showed better neurobehavioral recovery, alleviated neuronal injury, reduced infarct volume, and increased angiogenesis, as indicated by the elevated levels of brain-derived neurotrophic factor (BDNF), vascular endothelial growth factor (VEGF), and phosphorylated endothelial nitric oxide synthase (P-eNOS). Surprisingly, the beneficial effects of ta-VNS were weakened after PPAR-γ silencing. Conclusions. Our results suggest that PPAR-γ is a potential mediator of ta-VNS-induced angiogenesis and neuroprotection against cerebral I/R injury.

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Section: Inhibition Of Ppar-γ Weakens the Improvements Onsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

PPAR-γ Mediates Ta-VNS-Induced Angiogenesis and Subsequent Functional Recovery after Experimental Stroke in Rats

Zhang

et al. 2020

BioMed Research International

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“…Also, ACh-esterase inhibitor pyridostigmine increases VEGF-production in the left ventricle after MI, suggesting myocardial angiogenesis (Lataro et al, 2013) caused by an elevated ACh presence. VEGF levels, as well as microvessel density, were also higher in the penumbra of experimental cerebral ischemia in rats after VS (Jiang et al, 2016). These data suggest a relationship between the protective role of the parasympathetic nervous system and elevated VEGF levels in the area at risk after an ischemic period.…”

Section: Tablementioning

confidence: 60%

Effect of vagus nerve stimulation on tissue damage and function loss in a mouse myocardial ischemia-reperfusion model

Nederhoff

Fransen

Verlinde

et al. 2019

Autonomic Neuroscience

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In cardiac ischemia, acute inflammatory responses further increase the detrimental effect on myocardial tissue. Since vagus nerve stimulation (VS) attenuates inflammatory responsiveness this study examines the effect of VS on myocardial damage development in a cardiac ischemia-reperfusion (IR) mouse model. Methods: 54 male C57Bl/6j mice were subjected to an IR procedure with or without prior VS. The effects on inflammatory responsiveness, infarct size, cardiac function, neutrophils, lymphocytes and vascular endothelial growth factor (VEGF) in the infarcted myocardium were measured at 48 h after intervention. Group results were compared with unpaired Mann-Whitney or Kruskall-Wallis test. Results: A significant decrease in inflammatory responsiveness was not verified by decreased TNFα levels in blood from VS and IR treated mice. The percentage infarct size over area at risk was smaller in the group with VS + IR compared with IR (22.4 ± 10.2% vs 37.6 ± 9.0%, p = 0.003). The degree of the reduction in cardiac function was not different between the IR groups with or without VS and no group differences were found in amounts of neutrophils, CD3+ lymphocytes and VEGF in the reperfused mouse heart. Conclusion: The present study does not provide clear evidence of a reducing role for VS on cardiac function loss. This could mean that VS has a less inhibiting effect on myocardial inflammation than may be expected from the literature.

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“…AVN projects to the NTS, and importantly, this central vagal projection can now be accessed noninvasively via the external ear (Ay et al 2015;Hays 2016;Frangos et al 2015). AVN stimulation promoted postischemic functional recovery and angiogenesis, and upregulated expression of BDNF, endothelial nitric oxide synthase (eNOS), and vascular endothelial growth factor (VEGF) in the rat brain (Jiang et al 2016).…”

Section: Vagus Nerve Stimulation (Vns)-enhancing Plasticity In Neurommentioning

confidence: 99%

Dysfunctional Sensory Modalities, Locus Coeruleus, and Basal Forebrain: Early Determinants that Promote Neuropathogenesis of Cognitive and Memory Decline and Alzheimer’s Disease

Daulatzai

2016

Neurotox Res

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Sporadic Alzheimer's disease (AD) is a devastating neurodegenerative disorder. It is essential to unravel its etiology and pathogenesis. This should enable us to study the presymptomatic stages of the disease and to analyze and reverse the antemortem behavioral, memory, and cognitive dysfunction. Prima facie, an ongoing chronic vulnerability involving neural insult may lead normal elderly to mild cognitive impairment (MCI) and then to AD. Development of effective preventive and therapeutic strategies to thwart the disease pathology obviously requires a thorough delineation of underlying disruptive neuropathological processes. Our sensory capacity for touch, smell, taste, hearing, and vision declines with advancing age. Declines in different sensory attributes are considered here to be the primary "first-tier pathologies." Olfactory loss is among the first clinical signs of neurodegenerative diseases including AD and Parkinson's disease (PD). Sensory dysfunction in the aged promotes pathological disturbances in the locus coeruleus, basal forebrain, entorhinal cortex, hippocampus, and several key areas of neocortex and brainstem. Hence, sensory dysfunction is the pivotal factor that may upregulate cognitive and memory dysfunction. The age-related constellation of comorbid pathological factors may include apolipoprotein E (APOE) genotype, obesity, diabetes, hypertension, alcohol abuse, head trauma, and obstructive sleep apnea. The concepts and trajectories delineated here are the dynamic pillars of the current hypothesis presented-it postulates that the sensory decline, in conjunction with the above pathologies, is crucial in triggering neurodegeneration and promoting cognitive/memory dysfunction in aging and AD. The application of this thesis can be important in formulating new multifactorial preventive and treatment strategies (suggested here) in order to attenuate cognitive and memory decline and ameliorate pathological dysfunction in aging, MCI, and AD.

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Auricular vagus nerve stimulation promotes functional recovery and enhances the post-ischemic angiogenic response in an ischemia/reperfusion rat model

Cited by 50 publications

References 43 publications

PPAR-γ Mediates Ta-VNS-Induced Angiogenesis and Subsequent Functional Recovery after Experimental Stroke in Rats

PPAR-γ Mediates Ta-VNS-Induced Angiogenesis and Subsequent Functional Recovery after Experimental Stroke in Rats

Effect of vagus nerve stimulation on tissue damage and function loss in a mouse myocardial ischemia-reperfusion model

Dysfunctional Sensory Modalities, Locus Coeruleus, and Basal Forebrain: Early Determinants that Promote Neuropathogenesis of Cognitive and Memory Decline and Alzheimer’s Disease

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