Minocycline effects on cerebral edema: Relations with inflammatory and oxidative stress markers following traumatic brain injury in mice

Homsi, Shadi; Federico, Fabiola; Croci, Nicole; Palmier, B.; Plotkine, Michel; Marchand-Leroux, Catherine; Jafarian-Tehrani, Mehrnaz

doi:10.1016/j.brainres.2009.07.031

Cited by 133 publications

(104 citation statements)

References 54 publications

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“…To our knowledge, this is the first study to examine delayed immunosuppression at long-term injury time points, because other immunosuppressive treatments targeting anxiety-like behaviors have been administered before or within hours of injury. 34,37,38,[66][67][68][69] These results indicate that the persistence of post-traumatic anxiety may reflect chronic neuroinflammatory neuropathy, a possibility supported by the observation of activated microglia and astrocytes, key cells mediating inflammatory processes, many years after injury in long-term survivors of TBI. [9][10][11][12] Chronic post-traumatic neuroinflammation suggests the presence of a self-perpetuating positive feedback loop, possibly involving reactivation and further promotion of inflammatory mediators after injury in an inflammation-damage-inflammation cycle.…”

Section: Discussionmentioning

confidence: 70%

“…TBI in rodents also increases levels of activated glial cells and proinflammatory cytokines, [34][35][36][37][38] and administration of these cytokines increases anxiety-like behaviors. [29][30][31][32] The aim of the present study was therefore to determine whether neuroinflammation is associated with the long-term maintenance of post-traumatic anxiety in an animal model.…”

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confidence: 99%

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Reversal of Established Traumatic Brain Injury-Induced, Anxiety-Like Behavior in Rats after Delayed, Post-Injury Neuroimmune Suppression

Rodgers

Deming

Bercum

et al. 2014

Journal of Neurotrauma

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Traumatic brain injury (TBI) increases the risk of neuropsychiatric disorders, particularly anxiety disorders. Yet, there are presently no therapeutic interventions to prevent the development of post-traumatic anxiety or effective treatments once it has developed. This is because, in large part, of a lack of understanding of the underlying pathophysiology. Recent research suggests that chronic neuroinflammatory responses to injury may play a role in the development of post-traumatic anxiety in rodent models. Acute peri-injury administration of immunosuppressive compounds, such as Ibudilast (MN166), have been shown to prevent reactive gliosis associated with immune responses to injury and also prevent lateral fluid percussion injury (LFPI)-induced anxiety-like behavior in rats. There is evidence in both human and rodent studies that post-traumatic anxiety, once developed, is a chronic, persistent, and drug-refractory condition. In the present study, we sought to determine whether neuroinflammation is associated with the long-term maintenance of post-traumatic anxiety. We examined the efficacy of an anti-inflammatory treatment in decreasing anxiety-like behavior and reactive gliosis when introduced at 1 month after injury. Delayed treatment substantially reduced established LFPI-induced freezing behavior and reactive gliosis in brain regions associated with anxiety and continued neuroprotective effects were evidenced 6 months post-treatment. These results support the conclusion that neuroinflammation may be involved in the development and maintenance of anxiety-like behaviors after TBI.

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Section: Discussionmentioning

confidence: 70%

mentioning

confidence: 99%

Reversal of Established Traumatic Brain Injury-Induced, Anxiety-Like Behavior in Rats after Delayed, Post-Injury Neuroimmune Suppression

Rodgers

Deming

Bercum

et al. 2014

Journal of Neurotrauma

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Section: Discussionmentioning

confidence: 86%

“…Glial activation is normally neuroprotective (26,32); however, the chronic inflammatory responses and exaggerated proinflammatory cytokine levels observed following injury initiate neurotoxic processes resulting in secondary tissue damage (20,(33)(34)(35), neuronal death (29,(36)(37)(38), secondary injury cascades (39)(40)(41)(42)(43) and neuronal hyperexcitability (28, 34, 38, 44). There is substantial support for chronic inflammation following TBI.…”

Section: Post-traumatic Anxiety Is a Leading And Devastating Consequementioning

confidence: 99%

“…Several studies have reported increased anxiety-like behavior in rodent TBI models, [29][30][31][32] including increased conditioned 33 and unconditioned 34 fear responses to both learned and novel stimuli. TBI in rodents also increases levels of activated glial cells and proinflammatory cytokines, [34][35][36][37][38] and administration of these cytokines increases anxiety-like behaviors. [29][30][31][32] The aim of the present study was therefore to determine whether neuroinflammation is associated with the long-term maintenance of post-traumatic anxiety in an animal model.…”

Section: -4mentioning

confidence: 99%

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Targeting Microglia to Prevent Post-Traumatic Epilepsy

Barth¹

2014

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Department of Defense, Washington Headquarters Services, Directorate for Information Operations and Reports (0704-0188), 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302. Respondents should be aware that notwithstanding any other provision of law, no person shall be subject to any penalty for failing to comply with a collection of information if it does not display a currently valid OMB control number. PLEASE DO NOT RETURN YOUR FORM TO THE ABOVE ADDRESS. REPORT DATE July 2014 REPORT TYPE PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES)The Regents of the University of Colorado Boulder, CO 80303-1058 31 AND ADDRESS(ES) PERFORMING ORGANIZATION REPORT NUMBER SPONSORING / MONITORING AGENCY NAME(S) AND ADDRESS(ES) 10. SPONSOR/MONITOR'S ACRONYM(S) U.S. Army Medical Research and Materiel Command Fort Detrick, Maryland 21702-5012 SPONSOR/MONITOR'S REPORT NUMBER(S) DISTRIBUTION / AVAILABILITY STATEMENTApproved for Public Release; Distribution Unlimited SUPPLEMENTARY NOTES ABSTRACTThe purpose of this research project is to explore anti-epileptogenic strategies in and animal model of post-traumatic epilepsy (PTE) using lateral fluid percussion injury (LFPI). Our focus is on attenuating damaging effects of hyperexcitability in the brain induced by inflammation resulting from glial cell immune responses to trauma. We are exploring two drugs, MN166 and SLC022, that are known to suppress post-traumatic glial activation and thus inflammation to evaluate their effectiveness in preventing epileptogenesis in the LFPI model of PTE. In the first project year we developed a high-speed video/EEG recording and analysis system for rapid quantification of chronically recorded epileptiform activity in multiple (24-32) subjects. With this system we became expert in identifying epileptiform versus normal video/EEG activity in the rodent and discovered an important source of artifact currently being interpreted in other published reports as seizure activity. We developed a pilocarpine model of temporal lobe epilepsy to explore the effectiveness of glial cell (neuroimmune) attenuation in preventing or limiting epileptogenesis (development of epilepsy) in this rapidly developing model. We explored numerous changes in the LFPI model to produce earlier developing signs of epilepsy, increasing the probability of succeeding in our long-term study of epileptogenesis following traumatic brain injury. Perhaps the most important outcome of this work was the negative finding that much published work concerning PTE with the LFPI model has not properly examined controls. Both injured and uninjured rats displ...

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The role of bioactive lipids in attenuating the neuroinflammatory cascade in traumatic brain injury

Poblete

Arenas

Sanossian

et al. 2020

Ann Clin Transl Neurol

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Traumatic brain injury (TBI) is a major cause of morbidity, mortality, and economic burden. Despite this, there are no proven medical therapies in the pharmacologic management of TBI. A better understanding of disease pathophysiology might lead to novel approaches. In one area of increasing interest, bioactive lipids known to attenuate inflammation might serve as an important biomarker and mediator of disease after TBI. In this review, we describe the pathophysiology of inflammation following TBI, the actions of endogenous bioactive lipids in attenuating neuroinflammation, and their possible therapeutic role in the management of TBI. In particular, specialized pro‐resolving lipid mediators (SPMs) of inflammation represent endogenous compounds that might serve as important biomarkers of disease and potential therapeutic targets. We aim to discuss the current literature from animal models of TBI and limited human experiences that suggest that bioactive lipids and SPMs are mechanistically important to TBI recovery, and by doing so, aim to highlight the need for further clinical and translational research. Early investigations of dietary and parenteral supplementation of pro‐resolving bioactive lipids have been promising. Given the high morbidity and mortality that occurs with TBI, novel approaches are needed.

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Minocycline effects on cerebral edema: Relations with inflammatory and oxidative stress markers following traumatic brain injury in mice

Cited by 133 publications

References 54 publications

Reversal of Established Traumatic Brain Injury-Induced, Anxiety-Like Behavior in Rats after Delayed, Post-Injury Neuroimmune Suppression

Reversal of Established Traumatic Brain Injury-Induced, Anxiety-Like Behavior in Rats after Delayed, Post-Injury Neuroimmune Suppression

Targeting Microglia to Prevent Post-Traumatic Epilepsy

The role of bioactive lipids in attenuating the neuroinflammatory cascade in traumatic brain injury

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