Effects of N-Butylphthalide on the expressions of Nogo/NgR in rat brain tissue after carbon monoxide poisoning

Li, Qin; Cheng, Yongmei; Bi, Ming Jun; Kang, Hai; Qu, Yun; Lin, Hongyang; Guo, Yunliang; Zou, Yong

doi:10.1016/j.etap.2015.02.013

Cited by 21 publications

(21 citation statements)

References 22 publications

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“…Similarly, HIF-2α could be detected through 1-4 hours in serum after inhalation of CO. It reaches a peak level at the end of four hours and the increase lasts for 12-24 hours [7,16,17].…”

Section: Discussionmentioning

confidence: 95%

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The use of serum hypoxia-inducible factor two alpha levels and diagnostic values in adult carbon monoxide poisoning

Altıntop¹,

Tatlı²,

Karakükçü³

et al. 2018

Med-Science

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Carbon monoxide poisoning (COP) is a life-threatening intoxication which should be interfered immediately to be prevented from serious damages. The effect of carbon monoxide (CO) in the body at the cell level is mediated by a CO-releasing molecule. This molecule results in heme degradation via heme oxygenase. Because of the high affinity of CO on heme, many enzymes with biological signal transduction cause heme protein increase. Universally, this signal activation with similar enzymes and mechanisms are used in COP. The most widely used test is Carboxyhaemoglobin (COHb) in serum. The COHb is used as a standard parameter in the diagnosis of COP. COHb levels, are high after CO poisoning and decrease rapidly with oxygen therapy in the first four hours. So COHb is insufficient to demonstrate chronic ischemic damage of hypoxia. Hypoxia-inducible factors (HIFs) are the master regulators of oxygen homeostasis. The best known HIF isoforms in the literature are HIF-1ɑ and HIF-2ɑ. Recently, more data have found about selective HIF-2ɑ responsive genes and indicate the importance of this isoform in hypoxic gene regulation. The present study purposed to determine the change in HIF-2ɑ values in adult patients in diagnosing COP. A significant statistical correlation was found between (p=0.05) serum HIF-2ɑ levels and the first COHb level. HIF-2ɑ levels at 4th hour in COP patients were significantly higher like first COHb. HIF-2ɑ levels can be used as a new biomarker in long-term for monitoring COP patients.

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“…Similarly, HIF-2α could be detected through 1-4 hours in serum after inhalation of CO. It reaches a peak level at the end of four hours and the increase lasts for 12-24 hours [7,16,17].…”

Section: Discussionmentioning

confidence: 95%

“…Polymorphonuclear leukocytes increase and cause lipid peroxidation in the brain. This lipid peroxidation is responsible for the delayed neurological effects of COP [4,7]. In COP, the oxidative stress plays an important role in hypoxic-ischemic brain injury [5].…”

Section: Introductionmentioning

confidence: 99%

The use of serum hypoxia-inducible factor two alpha levels and diagnostic values in adult carbon monoxide poisoning

Altıntop¹,

Tatlı²,

Karakükçü³

et al. 2018

Med-Science

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“…However, whether they are the specific biomarkers for the occurrence and development of DEACMP is still unclear. Thus, the effective therapies are further limited by major gaps in our understanding of the fundamental processes that improve rehabilitate and prevent neurogenesis of brain damage in adults …”

Section: Introductionmentioning

confidence: 99%

“…Thus, the effective therapies are further limited by major gaps in our understanding of the fundamental processes that improve rehabilitate and prevent neurogenesis of brain damage in adults. 10 Fasudil is currently the only clinically approved Rock inhibitor 11 and has been widely used to alleviate symptoms of a range of CNS disorders, including subarachnoid haemorrhage, 12 spinal cord injuries, 13 cerebral stroke, 14 Parkinson's disease, 15 experimental autoimmune encephalomyelitis, 16 neuropathic pain and epilepsy. It has been reported that Fasudil could improve stroke protection and blood flow after cerebral ischaemia by increasing nitric oxide (NO) production and endothelium-derived NO synthase (eNOS) expression, 17 activating astrocyte secretion of granulocyte-colony stimulating factor (G-CSF), inhibiting glutamate induced neurotoxicity, 18 and mobilizing endogenous NSCs in vivo and differentiating the C17.2 neural progenitor cell line in vitro.…”

Section: Introductionmentioning

confidence: 99%

Fasudil alleviates brain damage in rats after carbon monoxide poisoning through regulating neurite outgrowth inhibitor/oligodendrocytemyelin glycoprotein signalling pathway

Wang

Guo

et al. 2019

Basic Clin Pharma Tox

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Carbon monoxide (CO) poisoning can lead to many serious neurological symptoms. Currently, there are no effective therapies for CO poisoning. In this study, rats exposed to CO received hyperbaric oxygen therapy, and those in the Fasudil group were given additional Fasudil injection once daily. We found that the escape latency in CO poisoning group (CO group) was significantly prolonged, the T1/Ttotal was obviously decreased, and the mean escape time and the active escape latency were notably extended compared with those in normal control group (NC group, P < 0.05). After administration of Fasudil, the escape latency was significantly shortened, T1/Ttotal was gradually increased as compared with CO group (>1 week, P < 0.05). Ultrastructural damage of neurons and blood‐brain barrier of rats was serious in CO group, while the structural and functional integrity of neuron and mitochondria maintained relatively well in Fasudil group. Moreover, we also noted that the expressions of neurite outgrowth inhibitor (Nogo), oligodendrocyte‐myelin glycoprotein (OMgp) and Rock in brain tissue were significantly increased in CO group, and the elevated levels of the three proteins were still observed at 2 months after CO poisoning. Fasudil markedly reduced their expressions compared with those of CO group (P < 0.05). In summary, the activation of Nogo‐OMgp/Rho signalling pathway is associated with brain injury in rats with CO poisoning. Fasudil can efficiently down‐regulate the expressions of Nogo, OMgp and Rock proteins, paving a way for the treatment of acute brain damage after CO poisoning.

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“…Researchers also reported that the HBO had significant effects on DEACMP [12]. Recently, N-Butylphthalide was found to have a neuroprotective role in brain damage after acute CO poisoning [13,14]. Therefore, we conducted this study to explore the effect of N-Butylphthalide and HBO on the cognitive dysfunction in patients with DEACMP.…”

Section: Introductionmentioning

confidence: 99%

Efficacy of N-Butylphthalide and Hyperbaric Oxygen Therapy on Cognitive Dysfunction in Patients with Delayed Encephalopathy After Acute Carbon Monoxide Poisoning

et al. 2017

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BackgroundDelayed encephalopathy after acute carbon monoxide (CO) poisoning (DEACMP) is one of the most serious complications after CO poisoning. This study was conducted to explore the efficacy of the combined application of N-Butylphthalide and hyperbaric oxygenation therapy (HBO) on cognitive dysfunction in patients with DEACMP.Material/MethodsA total of 184 patients with DEACMP were randomly assigned to either receive HBO or N-Butylphthalide and HBO. Meanwhile, all patients received conventional treatment. The total remission rate (RR) was used to assess the clinical efficacy. The Mini-Mental State Examination (MMSE) was used to assess the cognitive function, and the National Institutes of Health Stroke Scale (NIHSS) was used to assess the neurological function.ResultsFinally, there were 90 and 94 patients in the control and experimental groups, respectively. After eight weeks of treatment, the total RR in the experimental group (47.9%) was significantly higher than that in the control group (33.3%). Compared to the control group, significantly more patients in the experimental group had MMSE scores of 24–30. The lower NIHSS score in the experimental group showed that N-Butylphthalide had the effect of preservation and restoration of neurological function. No obvious drug toxicity or liver and kidney dysfunction was observed, and there was no significant change in the level of blood glucose and blood lipids.ConclusionsThese results indicated that the combined application of N-Butylphthalide and HBO could significantly improve the cognitive dysfunction of patients with DEACMP and have great clinical efficacy, which should be further studied.

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Effects of N-Butylphthalide on the expressions of Nogo/NgR in rat brain tissue after carbon monoxide poisoning

Cited by 21 publications

References 22 publications

The use of serum hypoxia-inducible factor two alpha levels and diagnostic values in adult carbon monoxide poisoning

The use of serum hypoxia-inducible factor two alpha levels and diagnostic values in adult carbon monoxide poisoning

Fasudil alleviates brain damage in rats after carbon monoxide poisoning through regulating neurite outgrowth inhibitor/oligodendrocytemyelin glycoprotein signalling pathway

Efficacy of N-Butylphthalide and Hyperbaric Oxygen Therapy on Cognitive Dysfunction in Patients with Delayed Encephalopathy After Acute Carbon Monoxide Poisoning

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