The Possible Damaged Mechanism and the Preventive Effect of Monosialotetrahexosylganglioside in a Rat Model of Cerebral Ischemia-Reperfusion Injury

Zhang, Jie; Fang, Xin; Zhou, Yiyi; Deng, Xia; Lü, Yi; Jiao, Li; Li, Shujuan; Wang, Bo; Xu, Renshi

doi:10.1016/j.jstrokecerebrovasdis.2015.02.008

Cited by 35 publications

(20 citation statements)

References 19 publications

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“…The toxic mechanism of ROS mainly includes: (1) acting on polyunsaturated fatty acids causes lipid peroxidation in mitochondrial membrane (Mukherjee et al, 2019); (2) inducing cross-linking of macromolecules such as DNA, RNA, polysaccharides and amino acids, then the crosslinked macromolecules lose their original activity or function (Li S. et al, 2019); (3) damaging endothelial cells and causing an increased permeability in blood-brain barrier due to their high reactivity to oxidized lipids and proteins (Wang Y. et al, 2019); (4) mediating inflammation and immune response by stimulating the expression of cytokines and adhesion molecules, leading to and aggravating brain tissue reperfusion injury ; (5) promoting polymerization and degradation of polysaccharide molecules. Free radicals can attack a wide range of nerve membranes and blood vessels that are rich in unsaturated fatty acids, triggering lipid peroxidation cascade effect, protein denaturation, polynucleotide strand breaks, base re-modification, cell structure integrity destruction, and thus the permeability, ion transport, and barrier functions of cell membrane are all seriously affected (Xing et al, 2018); and (6) leading to increased release of excitatory amino acid (EAA) that promotes the development of delayed neuron death after cerebral ischemia (Zhang et al, 2015a).…”

Section: Rosmentioning

confidence: 99%

Targeting Oxidative Stress and Inflammation to Prevent Ischemia-Reperfusion Injury

Xiong

et al. 2020

Front. Mol. Neurosci.

254

163

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The cerebral ischemia injury can result in neuronal death and/or functional impairment, which leads to further damage and dysfunction after recovery of blood supply. Cerebral ischemia/reperfusion injury (CIRI) often causes irreversible brain damage and neuronal injury and death, which involves many complex pathological processes including oxidative stress, amino acid toxicity, the release of endogenous substances, inflammation and apoptosis. Oxidative stress and inflammation are interactive and play critical roles in ischemia/reperfusion injury in the brain. Oxidative stress is important in the pathological process of ischemic stroke and is critical for the cascade development of ischemic injury. Oxidative stress is caused by reactive oxygen species (ROS) during cerebral ischemia and is more likely to lead to cell death and ultimately brain death after reperfusion. During reperfusion especially, superoxide anion free radicals, hydroxyl free radicals, and nitric oxide (NO) are produced, which can cause lipid peroxidation, inflammation and cell apoptosis. Inflammation alters the balance between pro-inflammatory and anti-inflammatory factors in cerebral ischemic injury. Inflammatory factors can therefore stimulate or exacerbate inflammation and aggravate ischemic injury. Neuroprotective therapies for various stages of the cerebral ischemia cascade response have received widespread attention. At present, neuroprotective drugs mainly include free radical scavengers, anti-inflammatory agents, and anti-apoptotic agents. However, the molecular mechanisms of the interaction between oxidative stress and inflammation, and their interplay with different types of programmed cell death in ischemia/reperfusion injury are unclear. The development of a suitable method for combination therapy has become a hot topic.

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Section: Rosmentioning

confidence: 99%

Targeting Oxidative Stress and Inflammation to Prevent Ischemia-Reperfusion Injury

Xiong

et al. 2020

Front. Mol. Neurosci.

254

163

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“…Given its good neuroprotective effects in animal experiments [165,[172][173][174][175][176][177][178][179], GM1 successfully attracted the attention of neurologists and began to be used in patients with acute ischemic stroke; however, its clinical efficacy still needs to be demonstrated. A systematic review of 12 controlled clinical trials involving about 2300 ischemic patients was published by Candelise and Ciccone in the Cochrane Stroke Group trials register [119].…”

Section: Gm1 In Ischemic Damage Of Adultsmentioning

confidence: 99%

GM1 Ganglioside Is A Key Factor in Maintaining the Mammalian Neuronal Functions Avoiding Neurodegeneration

Chiricozzi

Lunghi

Biase

et al. 2020

IJMS

123

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Many species of ganglioside GM1, differing for the sialic acid and ceramide content, have been characterized and their physico-chemical properties have been studied in detail since 1963. Scientists were immediately attracted to the GM1 molecule and have carried on an ever-increasing number of studies to understand its binding properties and its neurotrophic and neuroprotective role. GM1 displays a well balanced amphiphilic behavior that allows to establish strong both hydrophobic and hydrophilic interactions. The peculiar structure of GM1 reduces the fluidity of the plasma membrane which implies a retention and enrichment of the ganglioside in specific membrane domains called lipid rafts. The dynamism of the GM1 oligosaccharide head allows it to assume different conformations and, in this way, to interact through hydrogen or ionic bonds with a wide range of membrane receptors as well as with extracellular ligands. After more than 60 years of studies, it is a milestone that GM1 is one of the main actors in determining the neuronal functions that allows humans to have an intellectual life. The progressive reduction of its biosynthesis along the lifespan is being considered as one of the causes underlying neuronal loss in aged people and severe neuronal decline in neurodegenerative diseases. In this review, we report on the main knowledge on ganglioside GM1, with an emphasis on the recent discoveries about its bioactive component.

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“…During ischemic stroke, GM-1 and carnosine exert their neuroprotective effects by inhibiting macromolecular oxidation 36,37. UCP3 is an uncoupling protein (UCP) family member and regulates mitochondrial adenosine-triphosphate (ATP) and reactive oxygen species (ROS) production 38.…”

Section: Resultsmentioning

confidence: 99%

Compound porcine cerebroside and ganglioside injection attenuates cerebral ischemia–reperfusion injury in rats by targeting multiple cellular processes

Wang¹,

Zhang²,

Liang³

et al. 2017

NDT

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BackgroundCompound porcine cerebroside and ganglioside injection (CPCGI) is a neurotrophic drug used clinically to treat certain functional disorders of brain. Despite its extensive usage throughout China, the exact mechanistic targets of CPCGI are unknown. This study was carried out to investigate the protective effect of CPCGI against ischemic neuronal damage in rats with middle cerebral artery occlusion (MCAO) reperfusion injury and to investigate the neuroprotective mechanisms of CPCGI.Materials and methodsAdult male Sprague-Dawley rats were subjected to MCAO surgery for 2 hours followed by reperfusion. The rats were administered CPCGI once a day for 14 days after reperfusion, and behavioral tests were performed 1, 3, 7, and 14 days post MCAO. Hematoxylin–eosin staining was used to measure infarct volume, and immunohistochemical analysis was performed to determine the number of NeuN-positive neurons in the ischemic cortex penumbra. Finally, the relative expression levels of proteins associated with apoptosis (Bcl-2, Bax, and GADD45α), synaptic function (Synaptophysin, SNAP25, Syntaxin, and Complexin-1/2), and mitochondrial function (KIFC2 and UCP3) were determined by Western blot.ResultsCPCGI treatment reduced infarct size, decreased neurological deficit scores, and accelerated the recovery of somatosensory function 14 days after MCAO. In addition, CPCGI reduced the loss of NeuN-positive cells in the ischemic cortex penumbra. In the ischemic cortex, CPCGI treatment decreased GADD45α expression, increased the Bcl-2/Bax ratio, augmented Synaptophysin, SNAP25, and Complexin-1/2 expression, and increased the expression of KIFC2 and UCP3 compared with sham rats 14 days after MCAO reperfusion injury.ConclusionCPCGI displays neuroprotective properties in rats subjected to MCAO injury by inhibiting apoptosis and improving synaptic and mitochondrial function.

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The Possible Damaged Mechanism and the Preventive Effect of Monosialotetrahexosylganglioside in a Rat Model of Cerebral Ischemia-Reperfusion Injury

Cited by 35 publications

References 19 publications

Targeting Oxidative Stress and Inflammation to Prevent Ischemia-Reperfusion Injury

Targeting Oxidative Stress and Inflammation to Prevent Ischemia-Reperfusion Injury

GM1 Ganglioside Is A Key Factor in Maintaining the Mammalian Neuronal Functions Avoiding Neurodegeneration

Compound porcine cerebroside and ganglioside injection attenuates cerebral ischemia–reperfusion injury in rats by targeting multiple cellular processes

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The Possible Damaged Mechanism and the Preventive Effect of Monosialotetrahexosylganglioside in a Rat Model of Cerebral Ischemia-Reperfusion Injury

Cited by 35 publications

References 19 publications

Targeting Oxidative Stress and Inflammation to Prevent Ischemia-Reperfusion Injury

Targeting Oxidative Stress and Inflammation to Prevent Ischemia-Reperfusion Injury

GM1 Ganglioside Is A Key Factor in Maintaining the Mammalian Neuronal Functions Avoiding Neurodegeneration

Compound porcine cerebroside and ganglioside injection attenuates cerebral ischemia&ndash;reperfusion injury in rats by targeting multiple cellular processes

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Compound porcine cerebroside and ganglioside injection attenuates cerebral ischemia–reperfusion injury in rats by targeting multiple cellular processes