Neuroprotective effects of the β-carboline abecarnil studied in cultured cortical neurons and organotypic retinal cultures

2007 ◽  
Vol 52 (7) ◽  
pp. 1488-1495 ◽  
Author(s):  
Karsten Ruscher ◽  
Stefan Rzeczinski ◽  
Elisabeth Thein ◽  
Dorette Freyer ◽  
Ilya V. Victorov ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Neuroprotective Effects ◽  
Cultured Cortical Neurons ◽  
Retinal Cultures

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 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.

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).

scholarly journals The Neuroprotective Effects of SIRT1 on NMDA-Induced Excitotoxicity

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Xiaorong Yang ◽  
Peipei Si ◽  
Huaping Qin ◽  
Litian Yin ◽  
Liang-Jun Yan ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Living Cells ◽  
Cellular Aging ◽  
Double Staining ◽  
Inhibitory Effects ◽  
Neuroprotective Effects ◽  
Cultured Cortical Neurons ◽  
Silent Information Regulator 1 ◽  
Calcein Am ◽  
Important Therapeutic Target

Silent information regulator 1 (SIRT1), an NAD+-dependent deacetylase, is involved in the regulation of gene transcription, energy metabolism, and cellular aging and has become an important therapeutic target across a range of diseases. Recent research has demonstrated that SIRT1 possesses neuroprotective effects; however, it is unknown whether it protects neurons from NMDA-mediated neurotoxicity. In the present study, by activation of SIRT1 using resveratrol (RSV) in cultured cortical neurons or by overexpression of SIRT1 in SH-SY5Y cell, we aimed to evaluate the roles of SIRT1 in NMDA-induced excitotoxicity. Our results showed that RSV or overexpression of SIRT1 elicited inhibitory effects on NMDA-induced excitotoxicity including a decrease in cell viability, an increase in lactate dehydrogenase (LDH) release, and a decrease in the number of living cells as measured by CCK-8 assay, LDH test, and Calcein-AM and PI double staining. RSV or overexpression of SIRT1 significantly improved SIRT1 deacetylase activity in the excitotoxicity model. Further study suggests that overexpression of SIRT1 partly suppressed an NMDA-induced increase in p53 acetylation. These results indicate that SIRT1 activation by either RSV or overexpression of SIRT1 can exert neuroprotective effects partly by inhibiting p53 acetylation in NMDA-induced neurotoxicity.

Neuroprotective effects of furopyrazole derivative of benzylindazole analogs on C2 ceramide-induced apoptosis in cultured cortical neurons

2009 ◽  
Vol 19 (12) ◽  
pp. 3225-3228 ◽  
Author(s):  
Yi-Chien Lin ◽  
Li-Chen Chou ◽  
Sheng-Chih Chen ◽  
Sheng-Chu Kuo ◽  
Li-Jiau Huang ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Neuroprotective Effects ◽  
Cultured Cortical Neurons ◽  
Induced Apoptosis

scholarly journals The cell-permeable mitochondrial calcium uniporter inhibitor Ru265 preserves cortical neuron respiration after lethal oxygen glucose deprivation and reduces hypoxic/ischemic brain injury

2020 ◽  
Vol 40 (6) ◽  
pp. 1172-1181 ◽  
Author(s):  
Robyn J Novorolsky ◽  
Matthew Nichols ◽  
Jong S Kim ◽  
Evgeny V Pavlov ◽  
Joshua J Woods ◽  
...  
Keyword(s):  
Brain Injury ◽  
Cortical Neurons ◽  
Therapeutic Potential ◽  
High Capacity ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Mitochondrial Calcium ◽  
Neuroprotective Effects ◽  
Sensorimotor Deficits ◽  
Cultured Cortical Neurons

The mitochondrial calcium (Ca2+) uniporter (MCU) mediates high-capacity mitochondrial Ca2+ uptake implicated in ischemic/reperfusion cell death. We have recently shown that inducible MCU ablation in Thy1-expressing neurons renders mice resistant to sensorimotor deficits and forebrain neuron loss in a model of hypoxic/ischemic (HI) brain injury. These findings encouraged us to compare the neuroprotective effects of Ru360 and the recently identified cell permeable MCU inhibitor Ru265. Unlike Ru360, Ru265 (2–10 µM) reached intracellular concentrations in cultured cortical neurons that preserved cell viability, blocked the protease activity of Ca2+-dependent calpains and maintained mitochondrial respiration and glycolysis after a lethal period of oxygen–glucose deprivation (OGD). Intraperitoneal (i.p.) injection of adult male C57Bl/6 mice with Ru265 (3 mg/kg) also suppressed HI-induced sensorimotor deficits and brain injury. However, higher doses of Ru265 (10 and 30 mg/kg, i.p.) produced dose-dependent increases in the frequency and duration of seizure-like behaviours. Ru265 is proposed to promote convulsions by reducing Ca2+ buffering and energy production in highly energetic interneurons that suppress brain seizure activity. These findings support the therapeutic potential of MCU inhibition in the treatment of ischemic stroke but also indicate that such clinical translation will require drug delivery strategies which mitigate the pro-convulsant effects of Ru265.

scholarly journals Protective Effects of Isoatriplicolide Tiglate from Paulownia coreana against Glutamate-induced Neurotoxicity in Primary Cultured Rat Cortical Cells

2010 ◽  
Vol 5 (6) ◽  
pp. 1934578X1000500
Author(s):  
Ill-Min Chung ◽  
Eun-Hye Kim ◽  
Hyun-Seok Jeon ◽  
Hyung-In Moon
Keyword(s):  
Cell Viability ◽  
Sesquiterpene Lactone ◽  
Aqueous Extract ◽  
Cortical Neurons ◽  
Protective Effects ◽  
Significant Protection ◽  
Cortical Cells ◽  
Neuroprotective Effects ◽  
Cultured Cortical Neurons

To examine the neuroprotective effects of Paulownia coreana, we tested its protection against the glutamate-induced neurotoxicity to primary cultured cortical neurons. An aqueous extract of the plants exhibited significant protection against glutamate-induced toxicity in primary cultured rat cortical cells. In order to clarify the neuroprotective mechanism(s) of this observed effect, isolation was performed to seek and identify active fractions and components. By such fractionation, one bioactive sesquiterpene lactone, isoatriplicolide tiglate, was isolated, which exhibited significant neuroprotective activities against glutamate-induced toxicity, exhibiting cell viability of about 50%, at concentrations ranging from 0.1 μM to 10 μM.

Sign in / Sign up

Export Citation Format

Share Document