scholarly journals Effect of 8-hydroxyquinoline and derivatives on human neuroblastoma SH-SY5Y cells under high glucose

PeerJ ◽  
2016 ◽  
Vol 4 ◽  
pp. e2389 ◽  
Author(s):  
Wilasinee Suwanjang ◽  
Supaluk Prachayasittikul ◽  
Virapong Prachayasittikul
Keyword(s):  
Cell Death ◽  
Intracellular Calcium ◽  
Signaling Pathways ◽  
High Glucose ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Human Neuroblastoma ◽  
Beneficial Effects ◽  
Therapeutic Development ◽  
Multifunctional Properties

8-Hydroxyquinoline and derivatives exhibit multifunctional properties, including antioxidant, antineurodegenerative, anticancer, anti-inflammatory and antidiabetic activities. In biological systems, elevation of intracellular calcium can cause calpain activation, leading to cell death. Here, the effect of 8-hydroxyquinoline and derivatives (5-chloro-7-iodo-8-hydroxyquinoline or clioquinol and 8-hydroxy-5-nitroquinoline or nitroxoline) on calpain-dependent (calpain-calpastatin) pathways in human neuroblastoma (SH-SY5Y) cells was investigated. 8-Hydroxyquinoline and derivatives ameliorated high glucose toxicity in SH-SY5Y cells. The investigated compounds, particularly clioquinol, attenuated the increased expression of calpain, even under high-glucose conditions. 8-Hydroxyquinoline and derivatives thus adversely affected the promotion of neuronal cell death by high glucose via the calpain-calpastatin signaling pathways. These findings support the beneficial effects of 8-hydroxyquinolines for further therapeutic development.

Inability to restore resting intracellular calcium levels as an early indicator of delayed neuronal cell death

1995 ◽  
Vol 690 (2) ◽  
pp. 145-156 ◽  
Author(s):  
David D. Limbrick ◽  
Severn B. Churn ◽  
Sompong Sombati ◽  
Robert J. DeLorenzo
Keyword(s):  
Cell Death ◽  
Intracellular Calcium ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Early Indicator ◽  
Delayed Neuronal Cell Death

scholarly journals The The Effects of Centella asiatica Extract (CAE) on Methamphetamine-Induced Neurotoxicity via Human Neuroblastoma Cell Line

2021 ◽  
Vol 16 ◽  
pp. 1-9
Author(s):  
Mazatulikhma Mat Zain Mat Zain ◽  
Nursyamila Shamsuddin ◽  
Mohd Shihabuddin Ahmad Noorden
Keyword(s):  
Cell Death ◽  
Neuroblastoma Cell ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Centella Asiatica ◽  
Human Neuroblastoma Cell ◽  
Asiatic Acid ◽  
Dependent Manner ◽  
Human Neuroblastoma

Methamphetamine (METH) was reported to caused neurotoxicity and cell death, in vitro. Centella asiatica or ‘pegaga’ is a native tropical herb with antioxidant and neuroprotective activities. Although the effects of Centella asiatica against oxidative stress and neuronal cell death have been reported in previous studies, however, the potential effects of Centella asiatica against psychostimulant methamphetamine (METH) are limited. Therefore, this study was aimed to evaluate the effects of Centella asiatica extract (CAE) against METH on all-trans retinoic acid, RA-differentiated human neuroblastoma, SH-SY5Y cells. The RA-differentiated SH-SY5Y cells were used to resemble dopaminergic neuronal-like cells. Cell viability was quantitatively assessed by 3-(4,5-dimethylthiazol-2-yl)-2 tetrazolium bromide, MTS assay.  CAE at varying concentrations from 1pg/mL to 1mg/mL significantly decreased the viability of the undifferentiated SH-SY5Y cells in a concentration-dependent manner. At 1mg/mL of CAE, significantly increased the viability of differentiated SH-SY5Y cells. Meanwhile, CAE at 100µg/mL and 1mg/mL significantly reversed the METH-induced neuronal cell death. The results revealed that promising treatment of CAE on METH-induced neurotoxicity is mediated by its high content of asiaticoside, asiatic acid, madecassoside and madecassic acid. Taken together, this study may suggest CAE as a potential therapeutic treatment for METH-induced neurotoxicity, in vitro.

scholarly journals Momordica charantia Ethanol Extract Attenuates H2O2-Induced Cell Death by Its Antioxidant and Anti-Apoptotic Properties in Human Neuroblastoma SK-N-MC Cells

Nutrients ◽  
2018 ◽  
Vol 10 (10) ◽  
pp. 1368 ◽  
Author(s):  
Kkot Kim ◽  
SeonAh Lee ◽  
Inhae Kang ◽  
Jung-Hee Kim
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Ethanol Extract ◽  
Momordica Charantia ◽  
Mitogen Activated Protein Kinase ◽  
Cellular Damage ◽  
Protective Effects ◽  
Human Neuroblastoma

Oxidative stress, which is induced by reactive oxygen species (ROS), causes cellular damage which contributes to the pathogenesis of neurodegenerative diseases. Momordica charantia (MC), a traditional medicinal plant, is known to have a variety of health benefits, such as antidiabetic, anti-inflammatory, and antioxidant effects. However, it is unknown whether MC has protective effects against oxidative stress-induced neuronal cell death. The aim of this study was to investigate the potential action of MC on oxidative stress induced by H2O2. First, we tested whether the pretreatment of Momordica charantia ethanol extract (MCEE) attenuates H2O2-induced cell death in human neuroblastoma SK-N-MC cells. MCEE pretreatment significantly improved cell viability and apoptosis that deteriorated by H2O2. Further, MCEE ameliorated the imbalance between intracellular ROS production and removal through the enhancement of the intracellular antioxidant system. Intriguingly, the inhibition of apoptosis was followed by the blockage of mitochondria-dependent cell death cascades and suppression of the phosphorylation of the mitogen-activated protein kinase signaling (MAPKs) pathway by MCEE. Taken together, MCEE was shown to be effective in protecting against H2O2-induced cell death through its antioxidant and anti-apoptotic properties.

scholarly journals High Glucose-Induced PC12 Cell Death by Increasing Glutamate Production and Decreasing Methyl Group Metabolism

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Minjiang Chen ◽  
Hong Zheng ◽  
Tingting Wei ◽  
Dan Wang ◽  
Huanhuan Xia ◽  
...  
Keyword(s):  
Amino Acids ◽  
Cell Death ◽  
Pc12 Cells ◽  
High Glucose ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Creatine Phosphate ◽  
Metabolic Changes ◽  
Extracellular Medium ◽  
Methyl Group

Objective. High glucose- (HG-) induced neuronal cell death is responsible for the development of diabetic neuropathy. However, the effect of HG on metabolism in neuronal cells is still unclear.Materials and Methods. The neural-crest derived PC12 cells were cultured for 72 h in the HG (75 mM) or control (25 mM) groups. We used NMR-based metabolomics to examine both intracellular and extracellular metabolic changes in HG-treated PC12 cells.Results. We found that the reduction in intracellular lactate may be due to excreting more lactate into the extracellular medium under HG condition. HG also induced the changes of other energy-related metabolites, such as an increased succinate and creatine phosphate. Our results also reveal that the synthesis of glutamate from the branched-chain amino acids (isoleucine and valine) may be enhanced under HG. Increased levels of intracellular alanine, phenylalanine, myoinositol, and choline were observed in HG-treated PC12 cells. In addition, HG-induced decreases in intracellular dimethylamine, dimethylglycine, and 3-methylhistidine may indicate a downregulation of methyl group metabolism.Conclusions. Our metabolomic results suggest that HG-induced neuronal cell death may be attributed to a series of metabolic changes, involving energy metabolism, amino acids metabolism, osmoregulation and membrane metabolism, and methyl group metabolism.

Characterization of Chikungunya virus infection in human neuroblastoma SH-SY5Y cells: Role of apoptosis in neuronal cell death

2012 ◽  
Vol 163 (2) ◽  
pp. 563-572 ◽  
Author(s):  
R. Dhanwani ◽  
M. Khan ◽  
A.S.B. Bhaskar ◽  
Rajpriya Singh ◽  
I.K. Patro ◽  
...  
Keyword(s):  
Cell Death ◽  
Virus Infection ◽  
Chikungunya Virus ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Human Neuroblastoma
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