Vagal Nerve Stimulation Attenuates Ischemia-Reperfusion Induced Retina Dysfunction in Acute Ocular Hypertension

Jiang, Meihui; Zhou, Yuyang; Hua, Dihao; Yang, Jiayi; Hu, Manli; Xing, Yiqiao

doi:10.3389/fnins.2019.00087

Cited by 5 publications

(4 citation statements)

References 64 publications

(74 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Inoue et al have found that stimulation of vagal afferents or efferents 24 h before renal ischemia markedly attenuated AKI and decreased systemic inflammation depending on α7 nicotinic acetylcholine receptor-(α7nAChR-) positive splenocytes [19]. In addition, VNS has been applied to treat I/R injury-induced inflammation and oxidative stress in multiple organs [11,16,19]. The VNS treatment in this study effectively ameliorated renal injury caused by I/R by reducing systemic inflammation and oxidative stress.…”

Section: Discussionmentioning

confidence: 62%

“…In this study, the left cervical vagosympathetic trunks of the rats were separated and stimulated (frequency 20 Hz, 0.1 ms duration) through a pair of TeflonR-coated silver wires (0.1 mm in diameter) with a special stimulator (S20, Jinjiang, Chengdu, China). The voltage necessary to achieve a 10% reduction in sinus rate was used as the threshold [11,16]. The VNS treatment was performed throughout the I/R process.…”

Section: Vns Treatmentmentioning

confidence: 99%

See 1 more Smart Citation

Vagus Nerve Stimulation Ameliorates Renal Ischemia-Reperfusion Injury through Inhibiting NF-κB Activation and iNOS Protein Expression

Wang

Deng

Lai

et al. 2020

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

Objective. In renal ischemia/reperfusion injury (RIRI), nuclear factor κB (NF-κB) initiates the expression of multiple genes involved in inflammatory disease. Inhibition of NF-κB-mediated inducible nitric oxide synthase (iNOS) expression can ameliorate RIRI. Vagus nerve stimulation (VNS) protects against various organs I/R injury. The present study was designed to elucidate the protective effect of VNS on RIRI and its influence on iNOS protein expression. Methods. Eighteen male Sprague-Dawley rats were randomly allocated into the sham group, the I/R group, and the VNS+I/R group, 6 rats per group. An RIRI model was induced by a right nephrectomy and blockade of the left renal pedicle vessels for 45 min. After 6 h of reperfusion, the blood samples and renal samples were collected. The VNS treatment was performed throughout the I/R process in the VNS+I/R group using specific parameters (20 Hz, 0.1 ms in duration, square waves) known to produce a small but reliable bradycardia. Blood was used for evaluation of renal function and inflammatory state. Renal injury was evaluated via TUNEL staining. Renal samples were harvested to evaluate renal oxidative stress, NF-κB p65 levels, and iNOS protein expression. Results. The VNS treatment reduces serum creatinine (Cr) and blood urea nitrogen (BUN) levels. Simultaneously, the levels of tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), and interleukin 1-beta (IL-1β) were significantly increased in the I/R group, but VNS treatment markedly ameliorated this inflammatory response. Furthermore, the VNS ameliorated oxidant stress and renal injury, indicated by a decrease in 3-nitrotyrosine (3-NT) formation and MDA and MPO levels and an increase in the SOD level compared to that in the I/R group. Finally, the VNS also significantly decreases NF-κB p65, iNOS, and nitrite/nitrate levels compared to that in the I/R group. Conclusion. Our findings indicate that NF-κB activation increased iNOS expression and promoted RIRI and that VNS treatment attenuated RIRI by inhibiting iNOS expression, oxidative stress, and inflammation via NF-κB inactivation.

show abstract

Section: Discussionmentioning

confidence: 62%

Section: Vns Treatmentmentioning

confidence: 99%

Vagus Nerve Stimulation Ameliorates Renal Ischemia-Reperfusion Injury through Inhibiting NF-κB Activation and iNOS Protein Expression

Wang

Deng

Lai

et al. 2020

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

show abstract

“…Notably, atVNS did not promote significant changes in c-Fos density in any of the thirty (fifteen per hemisphere) brain regions studied. Other previous reports found changes in c-Fos density after the electrostimulation, particularly an increase in the number of c-Fos+ cells, in areas of the brainstem (Huffman et al, 2019 ; Jiang et al, 2019 ; Katagiri et al, 2019 ). However, all these studies used percutaneous or invasive VNS approaches, or applied the stimulation longer times.…”

Section: Discussionmentioning

confidence: 82%

Auricular Transcutaneous Vagus Nerve Stimulation Acutely Modulates Brain Connectivity in Mice

Brambilla-Pisoni

Muñoz‐Moreno²,

Gallego-Amaro

et al. 2022

Front. Cell. Neurosci.

View full text Add to dashboard Cite

Brain electrical stimulation techniques take advantage of the intrinsic plasticity of the nervous system, opening a wide range of therapeutic applications. Vagus nerve stimulation (VNS) is an approved adjuvant for drug-resistant epilepsy and depression. Its non-invasive form, auricular transcutaneous VNS (atVNS), is under investigation for applications, including cognitive improvement. We aimed to study the effects of atVNS on brain connectivity, under conditions that improved memory persistence in CD-1 male mice. Acute atVNS in the cymba conchae of the left ear was performed using a standard stimulation protocol under light isoflurane anesthesia, immediately or 3 h after the training/familiarization phase of the novel object-recognition memory test (NORT). Another cohort of mice was used for bilateral c-Fos analysis after atVNS administration. Spearman correlation of c-Fos density between each pair of the thirty brain regions analyzed allowed obtaining the network of significant functional connections in stimulated and non-stimulated control brains. NORT performance was enhanced when atVNS was delivered just after, but not 3 h after, the familiarization phase of the task. No alterations in c-Fos density were associated with electrostimulation, but a significant effect of atVNS was observed on c-Fos-based functional connectivity. atVNS induced a clear reorganization of the network, increasing the inter-hemisphere connections and the connectivity of locus coeruleus. Our results provide new insights into the effects of atVNS on memory performance and brain connectivity extending our knowledge of the biological mechanisms of bioelectronics in medicine.

show abstract

“…VIP has been reported to protect retinal ganglion cells against glutamate excitotoxicity in vitro [178] and to reduce the retinal neurodegenerative effect of ischemia–reperfusion injury through an antioxidant action [179]. VIP may also mediate the reduction of t e inflammatory response and the improvement of retinal function induced by vagal stimulation in rats with acute ocular hypertension [180]. Recently, both PACAP and VIP have been shown to efficiently attenuate ischemic retinal degeneration induced by bilateral common carotid artery occlusion (BCCAO) when are bound to the cell penetrating peptide TAT and administered through eye drops [181].…”

Section: Vasoactive Intestinal Peptide and Pituitary Adenylate Cycmentioning

confidence: 99%

Neuroprotective Peptides in Retinal Disease

Cervia

Catalani

Casini

2019

JCM

View full text Add to dashboard Cite

In the pathogenesis of many disorders, neuronal death plays a key role. It is now assumed that neurodegeneration is caused by multiple and somewhat converging/overlapping death mechanisms, and that neurons are sensitive to unique death styles. In this respect, major advances in the knowledge of different types, mechanisms, and roles of neurodegeneration are crucial to restore the neuronal functions involved in neuroprotection. Several novel concepts have emerged recently, suggesting that the modulation of the neuropeptide system may provide an entirely new set of pharmacological approaches. Neuropeptides and their receptors are expressed widely in mammalian retinas, where they exert neuromodulatory functions including the processing of visual information. In multiple models of retinal diseases, different peptidergic substances play neuroprotective actions. Herein, we describe the novel advances on the protective roles of neuropeptides in the retina. In particular, we focus on the mechanisms by which peptides affect neuronal death/survival and the vascular lesions commonly associated with retinal neurodegenerative pathologies. The goal is to highlight the therapeutic potential of neuropeptide systems as neuroprotectants in retinal diseases.

show abstract

Vagal Nerve Stimulation Attenuates Ischemia-Reperfusion Induced Retina Dysfunction in Acute Ocular Hypertension

Cited by 5 publications

References 64 publications

Vagus Nerve Stimulation Ameliorates Renal Ischemia-Reperfusion Injury through Inhibiting NF-κB Activation and iNOS Protein Expression

Vagus Nerve Stimulation Ameliorates Renal Ischemia-Reperfusion Injury through Inhibiting NF-κB Activation and iNOS Protein Expression

Auricular Transcutaneous Vagus Nerve Stimulation Acutely Modulates Brain Connectivity in Mice

Neuroprotective Peptides in Retinal Disease

Contact Info

Product

Resources

About