scholarly journals Neuroprotective effects of genistein and folic acid on apoptosis of rat cultured cortical neurons induced by β-amyloid 31-35

2009 ◽  
Vol 102 (5) ◽  
pp. 655-662 ◽  
Author(s):  
Huan-Ling Yu ◽  
Li Li ◽  
Xiao-Hong Zhang ◽  
Li Xiang ◽  
Jie Zhang ◽  
...  
Keyword(s):  
Folic Acid ◽  
Cortical Neuron ◽  
Cortical Neurons ◽  
Tail Length ◽  
Underlying Mechanism ◽  
Pcr Analysis ◽  
Neuroprotective Effects ◽  
Regulated Expression ◽  
Cultured Cortical Neurons ◽  
Β Amyloid

Genistein and folic acid have been reported respectively to protect against the development of cognitive dysfunction; however, the underlying mechanism(s) for this protection remain unknown. In this report, the mechanism(s) contributing to the neuroprotective effects of genistein and folic acid were explored using rat cortical neuron cultures. We found that genistein and folic acid, both separately and collaboratively, increased cell viability and mitochondrial membrane potential in β-amyloid (Aβ) 31-35-treated neurons. Furthermore, reduced percentage of comet cells and shortened tail length were observed in the neurons treated with genistein or folic acid. A more significant reduction in tail length of the comet neurons was observed in the co-administered neurons. RT-PCR analysis of the cultured cortical neurons showed down-regulated expression of p53, bax and caspase-3, but up-regulated expression of bcl-2 in the three neuroprotective treatment groups compared with neurons from the Aβ31-35 solo-treated group. In a nuclear dyeing experiment using Hoechst 33342, we found that both genistein and folic acid prevent neuronal apoptosis. Collectively, these findings suggest that the mechanism underlying the neuroprotection of genistein and folic acid singly or in combination observed in cultured cortical neuron studies might be related to their anti-apoptotic properties.

scholarly journals Apamin Enhances Neurite Outgrowth and Regeneration after Laceration Injury in Cortical Neurons

Toxins ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 603
Author(s):  
Hyunseong Kim ◽  
Jin Young Hong ◽  
Junseon Lee ◽  
Wan-Jin Jeon ◽  
In-Hyuk Ha
Keyword(s):  
Phospholipase A2 ◽  
Neurite Outgrowth ◽  
Cortical Neurons ◽  
Neurological Diseases ◽  
Minor Component ◽  
Underlying Mechanism ◽  
Bee Venom ◽  
Dependent Manner ◽  
Neuroprotective Effects ◽  
Wide Range

Apamin is a minor component of bee venom and is a polypeptide with 18 amino acid residues. Although apamin is considered a neurotoxic compound that blocks the potassium channel, its neuroprotective effects on neurons have been recently reported. However, there is little information about the underlying mechanism and very little is known regarding the toxicological characterization of other compounds in bee venom. Here, cultured mature cortical neurons were treated with bee venom components, including apamin, phospholipase A2, and the main component, melittin. Melittin and phospholipase A2 from bee venom caused a neurotoxic effect in dose-dependent manner, but apamin did not induce neurotoxicity in mature cortical neurons in doses of up to 10 µg/mL. Next, 1 and 10 µg/mL of apamin were applied to cultivate mature cortical neurons. Apamin accelerated neurite outgrowth and axon regeneration after laceration injury. Furthermore, apamin induced the upregulation of brain-derived neurotrophic factor and neurotrophin nerve growth factor, as well as regeneration-associated gene expression in mature cortical neurons. Due to its neurotherapeutic effects, apamin may be a promising candidate for the treatment of a wide range of neurological diseases.

Neuroprotective effects of resveratrol on damages of mouse cortical neurons induced by β-amyloid through activation of SIRT1/Akt1 pathway

BioFactors ◽  
2013 ◽  
Vol 40 (2) ◽  
pp. 258-267 ◽  
Author(s):  
Jing Zhang ◽  
Xiaowen Feng ◽  
Jintao Wu ◽  
Hongyan Xu ◽  
Guibao Li ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Neuroprotective Effects ◽  
Β Amyloid

scholarly journals MicroRNA-26b/PTEN Signaling Pathway Mediates Glycine-Induced Neuroprotection in SAH Injury

Neurosurgery ◽  
2019 ◽  
Vol 66 (Supplement_1) ◽  
Author(s):  
Xingping Qin
Keyword(s):  
Neuronal Death ◽  
Cortical Neurons ◽  
Detection System ◽  
Neuroprotective Effect ◽  
Signal Pathway ◽  
Neuroprotective Effects ◽  
Mortality And Morbidity ◽  
Microglial Polarization ◽  
Show Evidence ◽  
Cultured Cortical Neurons

Abstract INTRODUCTION Glycine is a nonessential amino acid with known neuroprotective effects. Subarachnoid hemorrhage (SAH) is a form of stroke associated with high mortality and morbidity. Despite extensive research, the treatment for SAH is limited. The present study was designed to investigate the role of glycine in neuroprotection following SAH. We have previously demonstrated that glycine is involved in neuroprotection in intracerebral hemorrhage via the PTEN/AKT signal pathway. However, whether it has a role in inducing neuroprotection following SAH is not known. METHODS We established the SAH model, evaluated the SAH grade, neurological scores, brain water content, glycine-mediated C (FJC) staining, cell viability and LDH release, and did cortical neuron and microglia culture. Treatment was conducted by intracerebroventricular injection. Cultured cortical neurons and cultured cortical microglia were treated with standard ECS for 60 min and then treated with glycine (100 μM) for 60 min. Cell replacement medium was used for subsequent experiments. vPCR was performed on the Opticon 2 real-time polymerase chain reaction (PCR) detection system using the corresponding primers and SYBR gene PCR master mix. RESULTS In this present study, we show evidence of glycine mediated amelioration of neuronal death and brain edema following SAH via a novel pathway. Following SAH there is evidence of downregulation of S473 phosphorylation of AKT (p-AKT), which is reversed with glycine treatment. We also found that glycine-regulated neuroprotection following SAH via AKT activation. Glycine was shown to down-regulate PTEN by up-regulating miRNA-26b, followed by activation of AKT, resulting in inhibition of neuronal death. Inhibition of AKT, PTEN depletion or suppression of miRNA-26b blocked the neuroprotective effect of glycine. Glycine treatment also suppresses SAH-induced M1 microglial polarization and promotes anti-inflammation, which indirectly inhibits neuronal death. CONCLUSION Glycine has neuroprotective effects in SAH injury and is mediated by the miRNA-26b/PTEN/AKT signal pathway, which may be a therapeutic target for treatment of SAH injury.

scholarly journals CIRBP Ameliorates Neuronal Amyloid Toxicity via Antioxidative and Antiapoptotic Pathways in Primary Cortical Neurons

2020 ◽  
Vol 2020 ◽  
pp. 1-9 ◽  
Author(s):  
Fang Su ◽  
Shanshan Yang ◽  
Hongcai Wang ◽  
Zhenkui Qiao ◽  
Hong Zhao ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Rna Binding ◽  
Neuronal Loss ◽  
Underlying Mechanism ◽  
Protective Effects ◽  
Neuroprotective Effects ◽  
Primary Cortical Neurons ◽  
Amyloid Toxicity ◽  
Proapoptotic Protein ◽  
Ad Prevention

It is generally accepted that the amyloid β (Aβ) peptide toxicity contributes to neuronal loss and is involved in the initiation and progression of Alzheimer’s disease (AD). Cold-inducible RNA-binding protein (CIRBP) is reported to be a general stress-response protein, which is induced by different stress conditions. Previous reports have shown the neuroprotective effects of CIRBP through the suppression of apoptosis via the Akt and ERK pathways. The objective of this study is to examine the effect of CIRBP against Aβ-induced toxicity in cultured rat primary cortical neurons and attempt to uncover its underlying mechanism. Here, MTT, LDH release, and TUNEL assays showed that CIRBP overexpression protected against both intracellular amyloid β- (iAβ-) induced and Aβ25-35-induced cytotoxicity in rat primary cortical neurons. Electrophysiological changes responsible for iAβ-induced neuronal toxicity, including an increase in neuronal resting membrane potentials and a decrease in K+ currents, were reversed by CIRBP overexpression. Western blot results further showed that Aβ25-35 treatment significantly increased the level of proapoptotic protein Bax, cleaved caspase-3, and cleaved caspase-9 and decreased the level of antiapoptotic factor Bcl-2, but were rescued by CIRBP overexpression. Furthermore, CIRBP overexpression prevented the elevation of ROS induced by Aβ25-35 treatment by decreasing the activities of oxidative biomarker and increasing the activities of key enzymes in antioxidant system. Taken together, our findings suggested that CIRBP exerted protective effects against neuronal amyloid toxicity via antioxidative and antiapoptotic pathways, which may provide a promising candidate for amyloid-based AD prevention or therapy.

scholarly journals β-Amyloid 25-35 Peptide Reduces the Expression of Glutamine Transporter SAT1 in Cultured Cortical Neurons

2007 ◽  
Vol 33 (2) ◽  
pp. 248-256 ◽  
Author(s):  
Doungjai Buntup ◽  
Øivind Skare ◽  
Tom Tallak Solbu ◽  
Farrukh A. Chaudhry ◽  
Jon Storm-Mathisen ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Glutamine Transporter ◽  
Cultured Cortical Neurons ◽  
Β Amyloid

The AMPAR antagonist perampanel regulates neuronal necroptosis via Akt/GSK3β signaling after acute traumatic injury in cortical neurons

2020 ◽  
Vol 19 ◽  
Author(s):  
Tao Chen ◽  
Li-Kun Yang ◽  
Jie Zhu ◽  
Chun-Hua Hang ◽  
Yu-Hai Wang
Keyword(s):  
Traumatic Brain Injury ◽  
Protective Effect ◽  
Neuronal Death ◽  
Cortical Neurons ◽  
Therapeutic Potential ◽  
Traumatic Injury ◽  
Neuroprotective Effects ◽  
Stroke Models ◽  
Cultured Cortical Neurons

Background: Perampanel is a highly selective and non-competitive α-amino-3-hydroxy-5 -methyl-4-isoxazole propionate (AMPA) receptor (AMPAR) antagonist, which has been licensed as an orally administered antiepileptic drug in more than 55 countries. Recently, perampanel was found to exert neuroprotective effects in hemorrhagic and ischemic stroke models. Objective: In this study, the protective effect of perampanel was investigated. Method: The protective effect of perampanel was investigated in an in vitro traumatic neuronal injury (TNI) model in primary cultured cortical neurons. Conclusion: Our present data suggest that necroptosis plays a key role in the pathogenesis of neuronal death after TNI, and that perampanel might have therapeutic potential for patients with traumatic brain injury (TBI).

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