Effects of TNF-α and IFN-γ on Nitric Oxide-Induced Neurotoxicity in the Mouse Brain

Blais, Véronique; Rivest, Serge

doi:10.4049/jimmunol.172.11.7043

Cited by 49 publications

(47 citation statements)

References 40 publications

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“…NO has also been found to participate in Fas-mediated apoptosis in Jurkat cells and NO donor can induce apoptosis of murine thymocytes. Implication of this molecule in cellular toxicity has been suggested by the use of NO synthase inhibitors or knockout mice in different models of demyelinating and neurodegenerative diseases conditions (Blais and Rivest, 2004). The present study elucidated that acute reserpine injection in mice was associated with an elevation in the brain 8-OHDG and NO levels, as compared to the normal control.…”

Section: Discussionmentioning

confidence: 54%

Combination of resveratrol and fluoxetine in an acute model of depression in mice: Prevention of oxidative DNA fragmentation and monoamines degradation

Ahmed-Farid¹,

Ahmed²,

Saleh³

2016

J App Pharm Sci

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Resveratrol (RSV) is a natural polyphenol with diverse biological activities, including potent hepato-protective and antidepressant-like effects. Fluoxetine (FLX) is one of the most commonly prescribed antidepressant drugs, however; it has recently been postulated to induce liver damage. The present study aimed to assess the benefits of combining half the conventional doses of RSV and FLX in an acute reserpin e model of depression. Depression was induced in mice by a single i.p. reserpine injection. Oral administration of FLX (10 mg/kg), RSV (80 mg/kg) or their combination (FLX; 5 mg/kg and RSV; 40mg/kg) started one hour after reserpine injection and daily for the following two consecutive days. Behavioral tests were performed on the third day. Brain monoamines were assessed. Prevention of neurodegeneration and preservation potential of the DNA integrity were determined according to the brain nitric oxide and 8-hydroxy-2-deoxyguanosine contents. Effect on oxidative stress in both brain and liver was evaluated. Results revealed that combining half the dose of FLX with RSV showed antidepressant activity that was comparable to the effect of using FLX alone and in conclusion; we recommend that further investigations should be conducted to assess the applicability of using combinations of RSV and FLX to treat depression.

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Section: Discussionmentioning

confidence: 54%

Combination of resveratrol and fluoxetine in an acute model of depression in mice: Prevention of oxidative DNA fragmentation and monoamines degradation

Ahmed-Farid¹,

Ahmed²,

Saleh³

2016

J App Pharm Sci

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“…On this subject, a study with transgenic TNF -knockout mice demonstrated that microglial TNF , a known pro-inflammatory cytokine, was critical in the resolution of an inflammatory response and excitotoxic cell death. In addition, while the lack of TNF reduced microglial activation within 6 hours, an exaggerated microglial activation was measured 4 days later [113]. These data have highlighted not only that a "dark side" of the glia exists, but that in some cases, preventing glial activation in the CNS is undesirable as it could amplify or create pathological pain.…”

Section: Pathological or Protective: A Hamleti-cal Question!mentioning

confidence: 82%

Role of Endocannabinoids in Neuron-Glial Crosstalk

Luongo¹,

Palazzo²,

Novellis³

et al. 2010

TOPAINJ

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Evidence shows bidirectional crosstalk between neurons and glia, suggesting that glia play an active role in synaptic plasticity leading to chronic pain. Importantly, gliosis has been implicated in the development and maintenance of hyperalgesia or allodynia following chronic inflammation or nerve injury. Anandamide (AEA) and 2-arachidonoylglycerol (2-AG), or the lipoamino acid N-arachydonoyldopamine (NADA), are fatty acid derivative neurotransmitters, named endocannabinoids (eCBs). These perform several biological actions, via the activation of cannabinoid type 1 and 2 (CB1/CB2) receptors belonging to the G-protein-coupled receptor family. The eCBs are produced on demand by neurons or glial cells and it has been suggested that they might be involved in the crosstalk between astrocytes, microglia, oligodendrocytes and neurons. In chronic pain, the modified glial or neural activity also seems to be associated with changes in eCB levels in pain processing areas either in the spinal cord or the brain. The activation of the eCB system in microglia or astrocytes could be crucial in modulating axonal growth and synaptogenesis at the base of neural phenotypic changes. Furthermore, changes in eCBs levels have been suggested to affect the destiny of cells: death or survival may depend on a specific pain condition. Thus, although eCBs are emerging as neurotransmitters responsible for the regulation of glia-neuron crosstalk in chronic pain, the precise mechanisms leading to eCB production, the origin and the timecourse of eCB release, the eCB release switch from one cell type to the other and their movement or catabolism across the glial or neural cell membrane nevertheless still remain unknown. These issues together with alternative eCB targets will be addressed in the current review.

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“…5B). The latter was estimated by immunohistochemistry using a primary Ab directed against the neuronal marker NeuN, which vanishes rapidly in degenerating neurons (29). As depicted in Fig.…”

Section: Role Of E 2 In a Mouse Model Of Viral Infectionmentioning

confidence: 99%

Estradiol Is Required for a Proper Immune Response to Bacterial and Viral Pathogens in the Female Brain

Soucy

Boivin

Labrie

et al. 2005

The Journal of Immunology

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120

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Although the neuroprotective effects of estrogens are well recognized, the exact mechanisms involved in the ability of these sex steroids to protect the cerebral tissue still remain unclear. We tested in our study the hypothesis that estradiol (E2) modulates the innate immune response and expression of genes encoding proteins that a provide survival signal to neurons during infection. Mice received a single systemic or cerebral injection of LPS to trigger a robust but transient inflammatory reaction in the brain. The endotoxin increased transcriptional activation of genes encoding TLR2, TNF-α, and IL-12 in microglial cells. Expression of these transcripts was largely inhibited in the brain of ovariectomized mice at time 24 h postchallenge. E2 replacement therapy totally rescued the ability of the endotoxin to trigger microglial cells and these permissive effects of E2 are mediated via the estrogen receptor (ER)α. Indeed, ERα-deficient mice exhibited an inappropriate reaction to LPS when compared with ERβ-deficient and wild-type mice. This defective innate immune response was also associated with a widespread viral replication and neurodegeneration in ovariectomized mice inoculated intranasally with HSV-2. These data provide evidence that interaction of E2 with their nuclear ERα plays a critical role in the control of cytokines involved in the transfer from the innate to adaptive immunity. This transfer is deviant in mice lacking E2, which allows pathogens to hide from immune surveillance and exacerbates neuronal damages during viral encephalitis.

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Effects of TNF-α and IFN-γ on Nitric Oxide-Induced Neurotoxicity in the Mouse Brain

Cited by 49 publications

References 40 publications

Combination of resveratrol and fluoxetine in an acute model of depression in mice: Prevention of oxidative DNA fragmentation and monoamines degradation

Combination of resveratrol and fluoxetine in an acute model of depression in mice: Prevention of oxidative DNA fragmentation and monoamines degradation

Role of Endocannabinoids in Neuron-Glial Crosstalk

Estradiol Is Required for a Proper Immune Response to Bacterial and Viral Pathogens in the Female Brain

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