scholarly journals Maintenance of the Neuroprotective Function of the Amino Group Blocked Fluorescence-Agmatine

2021 ◽  
Author(s):  
Sumit Barua ◽  
A Young Sim ◽  
Jong Youl Kim ◽  
Injae Shin ◽  
Jong Eun Lee
Keyword(s):  
Study Data ◽  
Amino Group ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Neuronal Viability ◽  
Crystallographic Study ◽  
Experimental Drug ◽  
Idiopathic Pain ◽  
Neuroprotective Function ◽  
Positively Charged

AbstractAgmatine, an endogenous derivative of arginine, has been found to be effective in treating idiopathic pain, convulsion, stress-mediated behavior, and attenuate the withdrawal symptoms of drugs like morphine. In the early stages of ischemic brain injury in animals, exogenous agmatine treatment was found to be neuroprotective. Agmatine is also considered as a putative neurotransmitter and is still an experimental drug. Chemically, agmatine is called agmatine 1-(4-aminobutyl guanidine). Crystallographic study data show that positively-charged guanidine can bind to the protein containing Gly and Asp residues, and the amino group can interact with the complimentary sites of Glu and Ser. In this study, we blocked the amino end of the agmatine by conjugating it with FITC, but the guanidine end was unchanged. We compared the neuroprotective function of the agmatine and agmatine-FITC by treating them in neurons after excitotoxic stimulation. We found that even the amino end blocked neuronal viability in the excitotoxic condition, by NMDA treatment for 1 h, was increased by agmatine-FITC, which was similar to that of agmatine. We also found that the agmatine-FITC treatment reduced the expression of nitric oxide production in NMDA-treated cells. This study suggests that even if the amino end of agmatine is blocked, it can perform its neuroprotective function.

The Development of Stem Cell-Based Treatment for Acute Ischemic Cerebral Injury

2020 ◽  
Vol 15 (6) ◽  
pp. 509-521
Author(s):  
Xiaojie Bai ◽  
Jun Xu ◽  
Tiantian Zhu ◽  
Yuanyuan He ◽  
Hong Zhang
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Brain Injury ◽  
Modern Medicine ◽  
Cerebral Injury ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Serious Disease ◽  
Neuroprotective Function ◽  
Effective Treatments

Acute ischemic brain injury is a serious disease that severely endangers the life safety of patients. Such disease is hard to predict and highly lethal with very limited effective treatments currently. Although currently, there exist treatments like drug therapy, hyperbaric oxygen therapy, rehabilitation therapy and other treatments in clinical practice, these are not significantly effective for patients when the situation is severe. Thus scientists must explore more effective treatments. Stem cells are undifferentiated cells with a strong potential of self-renewal and differentiate into various types of tissues and organs. Their emergence has brought new hopes for overcoming difficult diseases, further improving medical technology and promoting the development of modern medicine. Some combining therapies and genetically modified stem cell therapy have also been proven to produce obvious neuroprotective function for acute ischemic brain injury. This review is an introduction to the current research findings and discusses the definition, origin and classification of stem cells, as well as the future prospects of the stem cell-based treatment for acute ischemic cerebral injury.

Caspase-1-independent Maturation of IL-1? in Ischemic Brain Injury: is there a Role for Gelatinases?

2016 ◽  
Vol 16 (9) ◽  
pp. 729-737 ◽  
Author(s):  
Diana Amantea ◽  
Rossella Russo ◽  
Michelangelo Certo ◽  
Laura Rombolà ◽  
Annagrazia Adornetto ◽  
...  
Keyword(s):  
Brain Injury ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Caspase 1

Bioactivity of Marine Natural Product Xyloketals

2020 ◽  
Vol 17 ◽  
Author(s):  
Biswajit Panda ◽  
Amal Kumar Gooyee
Keyword(s):  
Natural Products ◽  
Marine Natural Product ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Activity Inhibition ◽  
Life Saving ◽  
Behavior Suppression ◽  
Major Emphasis ◽  
Made In

: Oceans can play a major role in supplying life-saving medicines in the world in future. Although considerable progress has been made in finding new medicines from marine sources, large efforts are still necessary to examine such molecules for clinical applications. Xyloketals are an important group of natural products with various powerful and prominent bioactivities such as inhibition of acetylcholine esterase, antioxidant activity, inhibition of L-calcium channels, radicalscavenging behavior, suppression of cell proliferation, reduction of neonatal hypoxic-ischemic brain injury, etc. This review describes the isolation and structural characterization of all xyloketal natural products giving major emphasis on their bioactivity.

scholarly journals Induction of Tertiary Phase Epileptiform Discharges after Postasphyxial Infusion of a Toll-Like Receptor 7 Agonist in Preterm Fetal Sheep

2021 ◽  
Vol 22 (12) ◽  
pp. 6593
Author(s):  
Kenta H.T. Cho ◽  
Mhoyra Fraser ◽  
Bing Xu ◽  
Justin M. Dean ◽  
Alistair J. Gunn ◽  
...  
Keyword(s):  
Moderate Hypertension ◽  
Epileptiform Activity ◽  
Ischemic Brain Injury ◽  
Toll Like Receptor ◽  
Fetal Sheep ◽  
Ischemic Brain ◽  
Tlr Agonists ◽  
Epileptiform Discharges ◽  
Subcortical Regions ◽  
Total Burden

Background: Toll-like receptor (TLR) agonists are key immunomodulatory factors that can markedly ameliorate or exacerbate hypoxic–ischemic brain injury. We recently demonstrated that central infusion of the TLR7 agonist Gardiquimod (GDQ) following asphyxia was highly neuroprotective after 3 days but not 7 days of recovery. We hypothesize that this apparent transient neuroprotection is associated with modulation of seizure-genic processes and hemodynamic control. Methods: Fetuses received sham asphyxia or asphyxia induced by umbilical cord occlusion (20.9 ± 0.5 min) and were monitored continuously for 7 days. GDQ 3.34 mg or vehicle were infused intracerebroventricularly from 1 to 4 h after asphyxia. Results: GDQ infusion was associated with sustained moderate hypertension that resolved after 72 h recovery. Electrophysiologically, GDQ infusion was associated with reduced number and burden of postasphyxial seizures in the first 18 h of recovery (p < 0.05). Subsequently, GDQ was associated with induction of slow rhythmic epileptiform discharges (EDs) from 72 to 96 h of recovery (p < 0.05 vs asphyxia + vehicle). The total burden of EDs was associated with reduced numbers of neurons in the caudate nucleus (r2 = 0.61, p < 0.05) and CA1/2 hippocampal region (r2 = 0.66, p < 0.05). Conclusion: These data demonstrate that TLR7 activation by GDQ modulated blood pressure and suppressed seizures in the early phase of postasphyxial recovery, with subsequent prolonged induction of epileptiform activity. Speculatively, this may reflect delayed loss of early protection or contribute to differential neuronal survival in subcortical regions.

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