Inhibition of Neuronal Nitric Oxide Synthase by Ethyl Pyruvate in Schwann Cells Protects Against Peripheral Nerve Degeneration

Chung, Hyung-Joo; Kim, Muwoong; Jung, Junyang; Jeong, Na Young

doi:10.1007/s11064-019-02830-4

Cited by 12 publications

(15 citation statements)

References 38 publications

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“…Our data show that EP attenuates TBI‐induced myelin loss and improves myelin regeneration, which may decrease axon loss and lead to neurological functional recovery. In accordance with our study, protective effects of EP were reported previously in models of peripheral nerve degeneration 16,17 . EP regulated the expression of the myelin‐related transcription factor, c‐Jun, and inhibited axonal degradation during Wallerian degeneration 17 .…”

Section: Discussionsupporting

confidence: 93%

“…In accordance with our study, protective effects of EP were reported previously in models of peripheral nerve degeneration 16,17 . EP regulated the expression of the myelin‐related transcription factor, c‐Jun, and inhibited axonal degradation during Wallerian degeneration 17 . In addition, EP inhibited oxidative stress and pro‐inflammatory cytokines, and exerted powerful protective effects on axonal damage and demyelination in vitro 18 …”

Section: Discussionsupporting

confidence: 91%

“…Ethyl pyruvate has undergone clinical safety trials and is considered safe at therapeutically relevant doses. In addition to the highlighted studies in brain, EP was reported to be protective against peripheral nerve degeneration in Schwann cells 17 . Thus, EP may be a promising candidate for demyelination diseases not only in central nervous system (CNS), but also in peripheral nervous system.…”

Section: Discussionmentioning

confidence: 99%

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Ethyl pyruvate improves white matter remodeling in rats after traumatic brain injury

Mao

Sun

et al. 2020

CNS Neurosci Ther

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Background Severe traumatic brain injury (TBI) results in long‐term neurological deficits associated with white matter injury (WMI). Ethyl pyruvate (EP) is a simple derivative of the endogenous energy substrate pyruvate with neuroprotective properties, but its role in recovery from WMI has not been explored. Aims This study examines the effect of EP treatment on rats following TBI using behavioral tests and white matter histological analysis up to 28 days post‐injury. Materials and Methods Anaesthetised adult rats were subjected to TBI by controlled cortical impact. After surgery, EP or Ringers solution (RS) was administrated intraperitoneally at 15 min after TBI and again at 12, 24, 36, 48, and 60 h after TBI. Sensorimotor deficits were evaluated up to day 21 after TBI by four independent tests. Immunofluorescence and transmission electron microscopy (TEM) were performed to assess white matter injury. Microglia activation and related inflammatory molecules were examined up to day 14 after TBI by immunohistochemistry or real‐time PCR. Results Here, we demonstrate that EP improves sensorimotor function following TBI as well as improves white matter outcomes up to 28 d after TBI, as shown by reduced myelin loss. Furthermore, EP administration during the acute phase of TBI recovery shifted microglia polarization toward the anti‐inflammatoryM2 phenotype, modulating the release of inflammatory‐related factors. Conclusion EP treatment may protect TBI‐induced WMI via modulating microglia polarization toward M2.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

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Ethyl pyruvate improves white matter remodeling in rats after traumatic brain injury

Mao

Sun

et al. 2020

CNS Neurosci Ther

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“…[20] Schwann cells are key glial cells in the peripheral nervous system (PNS), which regulate nerve degeneration, and their proliferation is one of the main phenotypes during peripheral neurodegenerative processes. [21] Therefore, we performed a cell viability assay to estimate the bioactivity of six compounds with respect to Schwann cell proliferation using the MTS assay. In concentration-dependent analysis, 3 a, 3 b, 3 i, and 7 a showed significant decreases in cell viability in the SW10 cell-line as a dedifferentiated Schwann cell, compared with those of 3 q and 5 a (see Supporting Information Figure S2).…”

Section: Communicationsmentioning

confidence: 99%

“…To refine their bioactivity characteristics, gross morphological screenings were performed with 3 a, 3 b, 3 i, and 7 a; these screens tested the compounds' inhibitory effects on peripheral neurodegenerative processes using transverse stripe in ex vivo sciatic nerve culture. [21] The sciatic nerves are one of the biggest peripheral nerves in the PNS, and their ex vivo culture is an effective tool for estimating the effects of drugs on peripheral neurodegenerative processes. Transverse stripes are bands present on the surface of peripheral nerves, and their disappearance is one of the main phenotypes of peripheral neurodegeneration.…”

Section: Communicationsmentioning

confidence: 99%

Organocatalytic Enantioselective [4+3]‐Cycloadditions of Azaoxyallyl Cations with 2‐Aminophenyl Enones

et al. 2021

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The first organocatalytic asymmetric [4 + 3]-cycloaddition of 2-aminophenyl α,β-unsaturated carbonyls with in situ generated azaoxyallyl cations was developed, and enantioenriched functionalized seven-membered 1,4-benzodiazepine-3ones were obtained in good yields and with excellent enantioselectivities. This approach was also extended to the first asymmetric [4 + 3]-cycloaddition of δ-hydroxy α,β-unsaturated carbonyls, affording 1,4-oxazepanes in one step under mild conditions. Several of the novel adducts demonstrated promising bioactivity in the prevention of peripheral nerve degeneration.

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Free radical biology in neurological manifestations: mechanisms to therapeutics interventions

Tripathi

Gupta

Sahu

et al. 2021

Environ Sci Pollut Res

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Recent advancements and growing attention about free radicals (ROS) and redox signaling enable the scientific fraternity to consider their involvement in the pathophysiology of inflammatory diseases, metabolic disorders, and neurological defects. Free radicals increase the concentration of reactive oxygen and nitrogen species in the biological system through different endogenous sources and thus increased the overall oxidative stress. An increase in oxidative stress causes cell death through different signaling mechanisms such as mitochondrial impairment, cell-cycle arrest, DNA damage response, inflammation, negative regulation of protein, and lipid peroxidation. Thus, an appropriate balance between free radicals and antioxidants becomes crucial to maintain physiological function. Since the 1brain requires high oxygen for its functioning, it is highly vulnerable to free radical generation and enhanced ROS in the brain adversely affects axonal regeneration and synaptic plasticity, which results in neuronal cell death. In addition, increased ROS in the brain alters various signaling pathways such as apoptosis, autophagy, inflammation and microglial activation, DNA damage response, and cell-cycle arrest, leading to memory and learning defects. Mounting evidence suggests the potential involvement of micro-RNAs, circular-RNAs, natural and dietary compounds, synthetic inhibitors, and heat-shock proteins as therapeutic agents to combat neurological diseases. Herein, we explain the mechanism of free radical generation and its role in mitochondrial, protein, and lipid peroxidation biology. Further, we discuss the negative role of free radicals in synaptic plasticity and axonal regeneration through the modulation of various signaling molecules and also in the involvement of free radicals in various neurological diseases and their potential therapeutic approaches.

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Inhibition of Neuronal Nitric Oxide Synthase by Ethyl Pyruvate in Schwann Cells Protects Against Peripheral Nerve Degeneration

Cited by 12 publications

References 38 publications

Ethyl pyruvate improves white matter remodeling in rats after traumatic brain injury

Ethyl pyruvate improves white matter remodeling in rats after traumatic brain injury

Organocatalytic Enantioselective [4+3]‐Cycloadditions of Azaoxyallyl Cations with 2‐Aminophenyl Enones

Free radical biology in neurological manifestations: mechanisms to therapeutics interventions

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