Nociceptive spinal cord neurons of laminae I–III exhibit oxidative stress damage during diabetic neuropathy which is prevented by early antioxidant treatment with epigallocatechin-gallate (EGCG)

Raposo, Diogo; Morgado, C.; Pereira-Terra, Patrícia; Tavares, Isaura

doi:10.1016/j.brainresbull.2014.12.004

Cited by 48 publications

(31 citation statements)

References 63 publications

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“…We used a Leica DM-6000 CS fluorescence microscope (Leica Instruments Inc., Wetzlar, Germany) to visualize the stained spinal sections, recorded images using a SPOT Xplorer Digital camera (Diagnostic Instruments, Inc., Sterling Heights, MI, USA), and then measured the pixel values of the immunoreactive-positive areas using Image J software (National Institutes of Health, Bethesda, MD, USA) with three sections per rat. Spinal neurons distributed over the superficial laminae (laminae I-III) respond to nociceptive stimuli, and these neurons directly contribute to the transmission of nociception [33]. Therefore, the superficial laminae have more crucial roles in neuropathic pain compared to the deep laminae.…”

Section: Methodsmentioning

confidence: 99%

“…Therefore, the superficial laminae have more crucial roles in neuropathic pain compared to the deep laminae. Thus, we quantified immunoreactivity for the targeted proteins in the superficial laminae, as described by previous studies in rodents with neuropathy [10, 33–35]. Immunofluorescence data is presented as a percentage change compared to the sham operation plus vehicle group, which were regarded as 100 %.…”

Section: Methodsmentioning

confidence: 99%

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Contributions of p38 and ERK to the antinociceptive effects of TGF-β1 in chronic constriction injury-induced neuropathic rats

Chen

Sung

et al. 2016

J Headache Pain

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BackgroundTransforming growth factor-βs (TGF-βs) are a group of multifunctional proteins that have neuroprotective roles in various experimental models. We previously reported that intrathecal (i.t.) injections of TGF-β1 significantly inhibit neuropathy-induced thermal hyperalgesia, spinal microglia and astrocyte activation, as well as upregulation of tumor necrosis factor-α. However, additional cellular mechanisms for the antinociceptive effects of TGF-β1, such as the mitogen-activated protein kinase (MAPK) pathway, have not been elucidated. During persistent pain, activation of MAPKs, especially p38 and extracellular signal-regulated kinase (ERK), have crucial roles in the induction and maintenance of pain hypersensitivity, via both nontranscriptional and transcriptional regulation. In the present study, we used a chronic constriction injury (CCI) rat model to explore the role of spinal p38 and ERK in the analgesic effects of TGF-β1.MethodsWe investigated the cellular mechanisms of the antinociceptive effects of i.t. injections of TGF-β1 in CCI induced neuropathic rats by spinal immunohistofluorescence analyses.ResultsThe results demonstrated that the antinociceptive effects of TGF-β1 (5 ng) were maintained at greater than 50 % of the maximum possible effect in rats with CCI for at least 6 h after a single i.t. administration. Thus, we further examined these alterations in spinal p38 and ERK from 0.5 to 6 h after i.t. administration of TGF-β1. TGF-β1 significantly attenuated CCI-induced upregulation of phosphorylated p38 (phospho-p38) and phosphorylated ERK (phospho-ERK) expression in the dorsal horn of the lumbar spinal cord. Double immunofluorescence staining illustrated that upregulation of spinal phospho-p38 was localized to neurons, activated microglial cells, and activated astrocytes in rats with CCI. Additionally, increased phospho-ERK occurred in activated microglial cells and activated astrocytes. Furthermore, i.t. administration of TGF-β1 markedly inhibited phospho-p38 upregulation in neurons, microglial cells, and astrocytes. However, i.t. injection of TGF-β1 also reduced phospho-ERK upregulation in microglial cells and astrocytes.ConclusionsThe present results demonstrate that suppressing p38 and ERK activity affects TGF-β1-induced analgesia during neuropathy.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Contributions of p38 and ERK to the antinociceptive effects of TGF-β1 in chronic constriction injury-induced neuropathic rats

Chen

Sung

et al. 2016

J Headache Pain

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“…Raposo et al demonstrated that early treatment with EGCG prevented oxidative stress damage (8-hydroxy-2′-deoxyguanosine) and neuronal hyperactivity in the spinal cord and ameliorated behavior related to diabetic neuropathy [40]. …”

Section: Effect Of Flavonoids On Neuronal Cell Death and Dysfunctionmentioning

confidence: 99%

Bioactive Compounds and Their Neuroprotective Effects in Diabetic Complications

2016

Nutrients

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Hyperglycemia, hyperlipidemia and impaired insulin signaling during the development of diabetes can cause diabetic complications, such as diabetic neuropathy, resulting in significant morbidity and mortality. Although various therapeutics are available for the treatment of diabetic neuropathy, no absolute cure exists, and additional research is necessary to comprehensively understand the underlying pathophysiological pathways. A number of studies have demonstrated the potential health benefits of bioactive compounds, i.e., flavonoids and vitamins, which may be effective as supplementary treatments for diabetes and its complications. In this review, we highlight the most recent reports about the mechanisms of action of bioactive compounds (flavonoids and vitamins) possessing potential neuroprotective properties in diabetic conditions. Additional clinical studies are required to determine the appropriate dose and duration of bioactive compound supplementation for neuroprotection in diabetic patients.

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“…(Cobacho et al, 2014;Ferreira and Menescal-de-Oliveira, 2014;Pan et al, 2008;Raposo et al, 2015;Thomson et al, 2006;Tuboly et al, 2015). Drugs affecting these systems may modulate the pain http://dx.doi.org/10.1016/j.brainresbull.2015.07.005 0361-9230/© 2015 Elsevier Inc. All rights reserved.…”

Section: Introductionmentioning

confidence: 96%

A new potent analgesic agent with reduced liability to produce morphine tolerance

Király¹,

Caputi²,

Hanuska³

et al. 2015

Brain Research Bulletin

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Nociceptive spinal cord neurons of laminae I–III exhibit oxidative stress damage during diabetic neuropathy which is prevented by early antioxidant treatment with epigallocatechin-gallate (EGCG)

Cited by 48 publications

References 63 publications

Contributions of p38 and ERK to the antinociceptive effects of TGF-β1 in chronic constriction injury-induced neuropathic rats

Contributions of p38 and ERK to the antinociceptive effects of TGF-β1 in chronic constriction injury-induced neuropathic rats

Bioactive Compounds and Their Neuroprotective Effects in Diabetic Complications

A new potent analgesic agent with reduced liability to produce morphine tolerance

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