2021
DOI: 10.4103/1673-5374.290899
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Neuroprotection by cattle encephalon glycoside and ignotin beyond the time window of thrombolysis in ischemic stroke

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Cited by 7 publications
(6 citation statements)
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“…With the emergence of a new type of brain injury drug, monosialotetrahexosylganglioside (GM1), the treatment for HIE has entered a new era. GM1 plays a positive role in the growth, differentiation, and regeneration of neurons [ 9 ] and has been widely used in the treatment of acute ischemic stroke, Alzheimer's disease, and other cerebrovascular diseases [ 10 , 11 ]. A study has shown that GM1 used in HIE treatment can improve the short-term clinical efficacy and reduce long-term neurodevelopmental disorders in neonates [ 12 ].…”
Section: Introductionmentioning
confidence: 99%
“…With the emergence of a new type of brain injury drug, monosialotetrahexosylganglioside (GM1), the treatment for HIE has entered a new era. GM1 plays a positive role in the growth, differentiation, and regeneration of neurons [ 9 ] and has been widely used in the treatment of acute ischemic stroke, Alzheimer's disease, and other cerebrovascular diseases [ 10 , 11 ]. A study has shown that GM1 used in HIE treatment can improve the short-term clinical efficacy and reduce long-term neurodevelopmental disorders in neonates [ 12 ].…”
Section: Introductionmentioning
confidence: 99%
“…However, the therapeutic strategies aimed at promoting endogenous neurogenesis face numerous challenges. First, there are a series of dramatic changes in the cellular microenvironment due to damage to the blood–brain barrier, excitotoxicity, neuroinflammation, acidosis, and the production of reactive oxygen species after stroke, which affect endogenous neurogenic processes [ 50 ]. The mechanisms underlying the activation, proliferation, migration, differentiation, and integration of NSCs after a stroke are complex and require further investigation.…”
Section: Discussionmentioning
confidence: 99%
“…Stroke leads to brain tissue necrosis, nerve cell death, and a loss of order in the intricate wiring of neurons, glial cells, and the vascular system [ 21 ]. Catastrophic changes in the cellular microenvironment caused by injury to the blood–brain barrier, excitotoxicity, mitochondrial dysfunction, oxidative stress, and neuroinflammation after stroke can affect the survival, differentiation, and neurogenesis of endogenous NSCs [ 50 ]. Increasing evidence has supported that ischemic stroke induces neurogenesis in multiple brain regions [ 51 , 52 ].…”
Section: Endogenous Neurogenesis Mechanism: An Approach To Restoring ...mentioning
confidence: 99%
“…Since excitotoxicity, oxidative stress and inflammatory mediators are essential for IS progression [33] , they provide a wide range of targets for neuroprotective therapy strategies. Neuroprotective agents, including human urokininogenase [46] , cattle encephalon glycoside and ignotin [47] , edaravone [48 , 49] , statins [50 , 51] and iron‐gallic acid coordination polymer nanodots [52] , exert diverse neuroprotective effects through various target mechanisms [45] .…”
Section: Overview Of Ismentioning
confidence: 99%