Lipoxin A4 attenuates brain damage and downregulates the production of pro-inflammatory cytokines and phosphorylated mitogen-activated protein kinases in a mouse model of traumatic brain injury

Luo, Chengliang; Li, Qianqian; Chen, Xiping; Zhang, Xin-Mu; Li, Liliang; Li, Bei‐Xu; Zhao, Ziqin; Tao, Luyang

doi:10.1016/j.brainres.2013.01.037

Cited by 60 publications

(38 citation statements)

References 37 publications

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“…However, we found that LXA4 down-regulated the levels of phospho-ERK1/2 and nuclear NF-kB-p65 in NHEKs treated with or without LPS. It has been reported that LXA4 and its analogs probably achieved anti-inflammatory effects via ERK1/2 and NF-kB signal transduction pathways [39][40][41]. In the cell cycle, we have found that the proteins movement between cyclin D1, phospho-ERK1/2 and NF-kB-p65 with p16INK4A was in opposite direction when NHEKs were exposed to LPS with or without pretreatment with LXA4.…”

Section: Discussionmentioning

confidence: 85%

Lipoxin A4 inhibits proliferation and inflammatory cytokine/chemokine production of human epidermal keratinocytes associated with the ERK1/2 and NF-κB pathways

Hu¹,

Liu²,

Wang³

et al. 2015

Journal of Dermatological Science

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Section: Discussionmentioning

confidence: 85%

Lipoxin A4 inhibits proliferation and inflammatory cytokine/chemokine production of human epidermal keratinocytes associated with the ERK1/2 and NF-κB pathways

Hu¹,

Liu²,

Wang³

et al. 2015

Journal of Dermatological Science

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“…Lipoxin A4, has recently proved highly efficacious in reducing lesion volumes, edema, cytokines, and apoptotic proteins in the brains of mice given a controlled cortical impact (CCI) injury, but again its introduction had to be done directly into the brain by i.c.v. injection (Luo, 2013). Likewise, mice subjected to brain damage by lateral fluid percussion injury (FLPI) showed marked improvements in neuro-behavioral function (e.g., rotarod) and suppressed neuro-inflammation responses (e.g., microglia activation), when intraperitoneal injected with resolvin D1 and resolvin E1 (Harrison, 2015); however, to see this effect, both prophylactic and postinjury administration of the drugs had to be done (i.e., 3 days before and after, at 5 μg/kg).…”

Section: Discussionmentioning

confidence: 99%

“…3) Resolve physical injuries to retina and brain, when injected into rats and mice (Serhan, 2008, 201 0;Luo, 2013;Harrison, 201 5).…”

Section: Electroretinography (Erg)mentioning

confidence: 99%

Evaluation of Novel Polyunsaturated Fatty Acid Derived Lipid Mediators of Inflammation to Ameliorate the Deleterious Effects of Blast Over Pressure on Eye and Brain Visual Processing Centers in Rats

DeMar¹

2015

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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 e» sting 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 , 1215 Jefferson Davis HighWay, Suite 1204, Adington, 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. Blast inj ury has emerged as arguably the greatest threat to warfighters in current theaters of operation, and is a leading cause of vision loss in military personnel due to non-penetrating traumatic inj uries to the eyes and brain visual centers, likely caused by blast shock waves. In light of the difficult lifelong disability that permanent loss of vision represents, we propose there is an urgent need for new drug therapies that can arrest progression of neuronal cell death in the eye (retina) and brain, as result of exposure to blast w aves. Our hypothesis is that novel omega-6 and omega-3 polyunsaturated fatty acid derived lipid mediators of inflammation, i.e. , lipoxins, neuroprotectins, and resolvins, will aid as drugs in healing of neurons critical to visual function after blast wave induced eye and brain inj uries. Using an adult rat model of blast w ave exposure, during the first phase of the study, we rigorously characterized the cellular and functional damage to the eyes (retinas) and brain visual centers, by electroretinography (ERG), visual discrimination behavioral testing, and histopathology. Blast w ave inj ury was carried out by placing the rats in a compressed air driven shock tube and exposing them, in a right side on orientation, once to a 20 psi (260Hz) blast over pressure wave. Rats were assessed at baseline and then 1, 7, and 14 days post-exposure. By 7 to 14 days out, blasted rats versus shams showed significantly decreased ERG waveform amplitudes of retinal response to a light flash stimulus for the right side eyes (-30% less; n = 15 vs.14), a trend for impaired ability to visually discern a cue light to earn food rewards (-30% less; n = 10 vs. 11 ), and significant neuronal cell degeneration within the right side retinas and both brain optic tracts (2 and 3-fold more, respectively ; n = 15 vs. 14 ). ERG and histopathology results significantly correlated with each other (r = -0.7). There also was a strong relationship between the retina and brain optic tract cell damage (r = 0.8). Overall, our findings demonstrate that blast w ave exposure leads to loss of vision in rats, likely through retinal cell death follow ed by anter...

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“…The only study published on this subject so far was carried out in mice subjected to a weight-drop model of TBI, in which the impact was directed to an exposed area of dura mater overlaying the cortex of the left cerebral hemisphere [82]. Injected into the ipsilateral lateral ventricle shortly after trauma, LXA4 was found to reduce BBB permeability, brain edema, and the extent of the lesion.…”

Section: Traumatic Brain Injurymentioning

confidence: 99%

Neuroprotective Effects of Lipoxin A4 in Central Nervous System Pathologies

Martini

Forner

Bento³

et al. 2014

BioMed Research International

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Many diseases of the central nervous system are characterized and sometimes worsened by an intense inflammatory response in the affected tissue. It is now accepted that resolution of inflammation is an active process mediated by a group of mediators that can act in synchrony to switch the phenotype of cells, from a proinflammatory one to another that favors the return to homeostasis. This new genus of proresolving mediators includes resolvins, protectins, maresins, and lipoxins, the first to be discovered. In this short review we provide an overview of current knowledge into the cellular and molecular interactions of lipoxins in diseases of the central nervous system in which they appear to facilitate the resolution of inflammation, thus exerting a neuroprotective action.

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Lipoxin A4 attenuates brain damage and downregulates the production of pro-inflammatory cytokines and phosphorylated mitogen-activated protein kinases in a mouse model of traumatic brain injury

Cited by 60 publications

References 37 publications

Lipoxin A4 inhibits proliferation and inflammatory cytokine/chemokine production of human epidermal keratinocytes associated with the ERK1/2 and NF-κB pathways

Lipoxin A4 inhibits proliferation and inflammatory cytokine/chemokine production of human epidermal keratinocytes associated with the ERK1/2 and NF-κB pathways

Evaluation of Novel Polyunsaturated Fatty Acid Derived Lipid Mediators of Inflammation to Ameliorate the Deleterious Effects of Blast Over Pressure on Eye and Brain Visual Processing Centers in Rats

Neuroprotective Effects of Lipoxin A4 in Central Nervous System Pathologies

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