The effect of granulocyte colony-stimulating factor administration on carbon monoxide neurotoxicity in rats

Gholami, Maryam; Moallem, Seyyed Adel; Abnous, Khalil; Yazdi, Seyyed Abbas Tabatabaee; Movassaghi, Ahmad Reza; Azizzadeh, Mohammad; Mohamadpour, Amir Hooshang

doi:10.3109/01480545.2012.737802

Cited by 20 publications

(10 citation statements)

References 54 publications

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“…In a pilot study, we showed that COHb levels were reduced to 60% under these conditions. In another study, we have shown that examining brain tissue slides of CO‐poisoned rats showed histopathological changes induced by CO poisoning (Ghorbani et al, ) indicating an efficient CO intoxication.…”

Section: Discussionmentioning

confidence: 90%

G‐CSF administration attenuates brain injury in rats following carbon monoxide poisoning via different mechanisms

Gholami

Mohammadpour

Abnous

et al. 2015

Environmental Toxicology

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Acute severe carbon monoxide (CO) poisoning induces hypoxia that leads to cardiovascular and nervous systems disturbances. Different complex mechanisms lead to CO neurotoxicity including lipid peroxidation, inflammatory and immune-mediated reactions, myelin degeneration and finally neuronal apoptosis and necrosis. Granulocyte colony-stimulating factor (G-CSF) is considered to be a novel neuroprotective agent. In this study, we evaluated the efficacy of G-CSF therapy on CO neurotoxicity in rats with acute CO poisoning. Rats were exposed to 3000 ppm CO in air (0.3%) for 1 h, and then different doses (50,100, and 150 µg/kg) of G-CSF or normal saline were administrated intraperitoneally. Water content of brain as an indicator for total edema and blood brain barrier integrity (Evans blue extravasation) were evaluated. Malondialydehyde was determined in order to evaluate the effect of G-CSF on CO-induced lipid peroxidation in brain tissues. Also, the effect of G-CSF on myeloperoxidase activity in the brain tissue was evaluated. The effect of G-CSF administration on induced apoptosis in the brain was measured using TUNEL method. To evaluate the level of MBP, STAT3 and pSTAT3 and HO-1 proteins and the effect of G-CSF on these proteins Western blotting was carried out. G-CSF reduced water content of the edematous poisoned brains (100 µg/kg) and BBB permeability (100 and 150 µg/kg) (P < 0.05). G-CSF (150 µg/kg) reduced the MDA level in the brain tissues (P < 0.05 as compared to CO poisoned animals). G-CSF did not decrease the MPO activity after CO poisoning in any doses. G-CSF significantly reduced the number of apoptotic neurons and Caspase 3 protein levels in the brain. Western blotting results showed that G-CSF treatment enhanced expression of HO-1 and MBP, STAT3 and pSTAT3 proteins in the brain tissues. Based on our results, a single dose of G-CSF immediately after CO poisoning significantly attenuates CO neurotoxicity via different mechanisms. © 2015 Wiley Periodicals, Inc. Environ Toxicol 32: 37-47, 2017.

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Section: Discussionmentioning

confidence: 90%

G‐CSF administration attenuates brain injury in rats following carbon monoxide poisoning via different mechanisms

Gholami

Mohammadpour

Abnous

et al. 2015

Environmental Toxicology

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“…However, peripheral administration of G-CSF has shown neuroprotective properties in carbon monoxide poisoning (Ghorbani et al, 2013), a Parkinson’s disease model (Frank et al, 2012), in focal cerebral ischemia (Hong et al, 2012), and in a TBI model (Acosta et al, 2014). Thus, a more robust response in G-CSF levels could be neuroprotective and so correlate with a better outcome.…”

Section: Discussionmentioning

confidence: 99%

“…It also mobilizes stem cells and several studies indicate that it has neuroprotective properties after its peripheral administration (Frank et al, 2012; Ghorbani et al, 2013; Hong et al, 2012). For example, G-CSF is neuroprotective against carbon monoxide toxicity and ischemia.…”

Section: Introductionmentioning

confidence: 99%

Assessing blood granulocyte colony-stimulating factor as a potential biomarker of acute traumatic brain injury in mice and humans

Banks

Dohi

Hansen

et al. 2016

Brain, Behavior, and Immunity

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Previous work has found that serum G-CSF was acutely elevated in mice 24 h but not one week after controlled cortical impact (CCI). The purpose of this study was to investigate whether blood G-CSF correlates with the elevated brain cytokines in mice after CCI and also if it correlates with traumatic brain injury (TBI) in humans. Here, we found in mice undergoing CCI, a procedure that induces direct injury to the brain, that serum G-CSF correlated directly or indirectly with several brain cytokines, indicating it is a useful marker for the neuroinflammation of TBI. A pilot study in humans (phase I, n = 19) confirmed that plasma G-CSF is acutely elevated on day 1 (p < 0.001) of TBI and has returned to baseline by one week. In a second human sample (phase II) (n = 80), we found plasma G-CSF peaks about 12 h after arriving in the emergency department (41.6 +/− 5.4 pg/ml). Aging was weakly associated (p < 0.05) with a less robust elevation in serum G-CSF, but there was no difference with gender. ISS, a measure of total severity of injury, correlated with the degree of elevation in serum G-CSF (r = .419; p < 0.05), but severity of head injury (via AIS) did not. The latter may have been because of the statistically narrow range of head injuries among our cases and the high number of cases diagnosed with closed head injury (a non-codable diagnosis). In conclusion, plasma G-CSF may be a useful biomarker of TBI, correlating with neuroinflammation in the animal model and in the human studies with time since injury and total severity of injury. As such, it may be useful in determining whether TBI has occurred within the last 24 h.

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“…A diverse group of other substances has been tested in animal studies and has shown possible benefit, including granulocyte colony-stimulating factor, nimodipine, fructose diphosphate, hyperoxygenated solution and edaravone [57-60]. An even more diverse group of substances has been shown to be effective in hypoxic/reperfusion injury.…”

Section: Pharmacological Treatmentsmentioning

confidence: 99%

Carbon monoxide poisoning in the 21st century

Chiew

Buckley

2014

Crit Care

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The world has experienced some very large shifts in the epidemiology of carbon monoxide poisoning, but it remains one of the most important toxicological global causes of morbidity and mortality. The diagnosis can be quickly confirmed with blood gases (pulse oximeters lack both sensitivity and specificity). Several strong predictors for serious neurological sequelae (prolonged loss of consciousness and elevated S100B) and reduced life expectancy (elevated troponin) are now reasonably well established. Despite this clearly defined high-risk group and extensive research into the pathophysiology, there has been little translation into better treatment. Much of the pathophysiological research has focused on hyperbaric oxygen. Yet it is apparent that clinical trials show little evidence for benefit from hyperbaric oxygen, and the most recent even raises the possibility of harm for repeated courses. More logical and promising potential antidotes have been under-researched, although recently both animal and small human studies suggest that erythropoietin may reduce S100B and prevent neurological sequelae. Major breakthroughs are likely to require further research on this and other treatments that may inhibit post-hypoxic inflammatory responses and apoptosis.

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The effect of granulocyte colony-stimulating factor administration on carbon monoxide neurotoxicity in rats

Cited by 20 publications

References 54 publications

G‐CSF administration attenuates brain injury in rats following carbon monoxide poisoning via different mechanisms

G‐CSF administration attenuates brain injury in rats following carbon monoxide poisoning via different mechanisms

Assessing blood granulocyte colony-stimulating factor as a potential biomarker of acute traumatic brain injury in mice and humans

Carbon monoxide poisoning in the 21st century

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