Safeguarding the brain from oxidative damage.

Oxidative stress imposes a substantial cellular burden on the brain and contributes to diverse neurodegenerative diseases. Various antioxidant signaling pathways have been implicated in oxidative stress and have a protective effect on brain cells by increasing the release of numerous enzymes and through anti-inflammatory responses to oxidative damage caused by abnormal levels of reactive oxygen species (ROS). Although many molecules evaluated as antioxidants have shown therapeutic potentials in preclinical studies, the results of clinical trials have been less than satisfactory.

Inhibiting Nav1.7 channels in pulpitis: An in vivo study on neuronal hyperexcitability.

Pulpitis constitutes a significant challenge in clinical management due to its impact on peripheral nerve tissue and the persistence of chronic pain. Despite its clinical importance, the correlation between neuronal activity and the expression of voltage-gated sodium channel 1.7 (Nav1.

Neuroprotective effects of N-acetylcysteine amide against oxidative injury in an aging model of organotypic hippocampal slice cultures.

Objectives: Oxidative stress produces neurotoxicity and has been associated with disorders of the nervous system. We observed the neuroprotective effects of N-acetylcysteine amide (NACA) against kainic acid (KA)-induced oxidative stress in aging organotypic hippocampal slice cultures (OHSCs).

Materials And Methods: We used 6-8-day-old rats for long-term cultured OHSCs (9 w).

Chronic Treatment of Ascorbic Acid Leads to Age-Dependent Neuroprotection against Oxidative Injury in Hippocampal Slice Cultures.

Increased oxidative damage in the brain, which increases with age, is the cause of abnormal brain function and various diseases. Ascorbic acid (AA) is known as an endogenous antioxidant that provides neuronal protection against oxidative damage. However, with aging, its extracellular concentrations and uptake decrease in the brain.

Neuroprotection from Excitotoxic Injury by Local Administration of Lipid Emulsion into the Brain of Rats.

Lipid emulsion was recently shown to attenuate cell death caused by excitotoxic conditions in the heart. There are key similarities between neurons and cardiomyocytes, such as excitability and conductibility, which yield vulnerability to excitotoxic conditions. However, systematic investigations on the protective effects of lipid emulsion in the central nervous system are still lacking.

Neuroprotective effects of a protein tyrosine phosphatase inhibitor against hippocampal excitotoxic injury.

Neuronal excitotoxicity is the neuronal cell death arising from prolonged exposure to glutamate and the associated excessive influx of ions into the cell. Sodium orthovanadate (NaVO,) competitively inhibits the protein tyrosine phosphatases that affect intracellular protein phosphorylation. No study has examined the role of protein tyrosine phosphatases in kainic acid (KA)-induced excitotoxic injury using sodium orthovanadate.

Inhibition of Mammalian Target of Rapamycin (mTOR) Signaling in the Insular Cortex Alleviates Neuropathic Pain after Peripheral Nerve Injury.

Injury of peripheral nerves can trigger neuropathic pain, producing allodynia and hyperalgesia via peripheral and central sensitization. Recent studies have focused on the role of the insular cortex (IC) in neuropathic pain. Because the IC is thought to store pain-related memories, translational regulation in this structure may reveal novel targets for controlling chronic pain.

Spinal cord fusion with PEG-GNRs (TexasPEG): Neurophysiological recovery in 24 hours in rats.

Background: The GEMINI spinal cord fusion protocol has been developed to achieve a successful cephalosomatic anastomosis. Here, for the first time, we report the effects of locally applied water-soluble, conductive PEG(polyethylene glycol)ylated graphene nanoribbons (PEG-GNRs) on neurophysiologic conduction after sharp cervical cord transection in rats. PEG-GNRs were produced by the polymerization of ethylene oxide from anion-edged graphene nanoribbons.

Neuroprotective effects of okadaic acid following oxidative injury in organotypic hippocampal slice culture.

Oxidative stress produces neurotoxicity often related with various CNS disorders. A phosphatase inhibitor enhances the actions of the signaling kinases. Protein kinases mediated-action shows the neural protection in brain injury.

Effects of human mesenchymal stem cell transplantation combined with polymer on functional recovery following spinal cord hemisection in rats.

The spontaneous axon regeneration of damaged neurons is limited after spinal cord injury (SCI). Recently, mesenchymal stem cell (MSC) transplantation was proposed as a potential approach for enhancing nerve regeneration that avoids the ethical issues associated with embryonic stem cell transplantation. As SCI is a complex pathological entity, the treatment of SCI requires a multipronged approach.

Optical imaging of somatosensory evoked potentials in the rat cerebral cortex after spinal cord injury.

Optical imaging techniques have made it possible to monitor neural activity and to determine its spatiotemporal patterns. Traumatic spinal cord injury (SCI) results in both the death of gray matter neurons and the disruption of ascending and descending white matter tracts at the injury site, leading to the loss of motor and sensory functions. In this study, we monitored and compared cortical responses to the stimulation of sensory tracts in normal control and spinal-cord-injured rats using an optical imaging technique based on a voltage-sensitive dye (VSD).

Neuroprotective effects of FK506 against excitotoxicity in organotypic hippocampal slice culture.

FK506 has been originally classified as an immunosuppressant and is known to exhibit neurotrophic actions in vitro and protective effects on some neurological conditions. We investigated the neuroprotective effects of FK506 on kainic acid (KA)-induced neuronal death in organotypic hippocampal slice cultures (OHSCs). After an 18 h KA (5 microM) treatment, significantly neuronal death was detected in the CA3 region using propidium iodide staining.

Behavioral characteristics of a mouse model of cancer pain.

Pain is a major symptom in cancer patients, and most cancer patients with advanced or terminal cancers suffer from chronic pain related to treatment failure and/or tumor progression. In the present study, we examined the development of cancer pain in mice. Murine hepatocarcinoma cells, HCa-1, were inoculated unilaterally into the thigh or the dorsum of the foot of male C3H/HeJ mice.

Effects of methylprednisolone on the neural conduction of the motor evoked potentials in spinal cord injured rats.

Methylprednisolone(MP), a glucocorticoid steroid, has an anti-inflammatory action and seems to inhibit the formation of oxygen free radicals produced during lipid peroxidation in a spinal cord injury(SCI). However, the effects of MP on the functional recovery after a SCI is controversial. The present study was conducted to determine the effects of MP on the recovery of neural conduction following a SCI.

Injury in the spinal cord may produce cell death in the brain.

Functional deficits after spinal cord injury have originated not only from the direct physical damage itself, but from the secondary biochemical and pathological changes. Apoptotic cell death has been seen around the periphery of an injured site and has been known to ultimately progress to necrosis and infarction. We have initiated the present study focusing on the role of apoptosis in the secondary injury of the brain after acute spinal cord injury (SCI), and conducted a series of experiments, the study examining the morphological changes in the brain following the spinal injury.