Assessment of neuroprotective effects of Gallic acid against glutamate-induced neurotoxicity in primary rat cortex neuronal culture
Glutamate excitotoxicity plays a crucial role in the pathogenesis behind the development and progression of several neurodegenerative diseases. The study aimed to investigate the neuroprotective activity of Gallic acid (GA) against glutamate-induced neurotoxicity in primary rat cortex neurons (RCN)....
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| Published in | Neurochemistry international Vol. 121; pp. 50 - 58 |
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| Main Authors | , , |
| Format | Journal Article |
| Language | English |
| Published |
England
Elsevier Ltd
01.12.2018
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0197-0186 1872-9754 1872-9754 |
| DOI | 10.1016/j.neuint.2018.10.011 |
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| Abstract | Glutamate excitotoxicity plays a crucial role in the pathogenesis behind the development and progression of several neurodegenerative diseases. The study aimed to investigate the neuroprotective activity of Gallic acid (GA) against glutamate-induced neurotoxicity in primary rat cortex neurons (RCN). Treated the RCNs with GA 25 & 50 μg/ml for 2 h and later treated the cells with 100 μM glutamate (GLU) and incubated for 24 h at 37 °C. The results demonstrated that, the GA improved the antioxidant profile in the cortex neurons and inhibited the production of the proinflammatory cytokine. GA also maintained the Ca2+ homeostasis, IGF-1 expression, and protected the neurons from glutamate-induced neuronal toxicity. The neuroprotective activity of GA has further confirmed from the results of N-acetylaspartate and expression of microtubule-associated protein-2 expression. The reports suggest that, GA is significantly attenuated the glutamate-induced neurotoxicity and protected neurons from various chemical events that are involved in the pathogenesis of neurotoxicity.
•Glutamate excitotoxicity is a major pathogenesis behind the development and progression of neurodegenerative diseases.•Glutamate-induced neurotoxicity in RCN is mediated through the formation of free radicles and proinflammatory cytokine.•Glutamate treatment also caused an alteration in Ca2+ homeostasis and decline in IGF-1 level.•Observed a down-regulation of MAP-2 expression and NAA concentration in glutamate treated rat cortex neurons.•Treatment with GA improved the antioxidant status in neurons and inhibited proinflammatory cytokine production.•GA also maintained the Ca2+ homeostasis, IGF-1 expression, and protected neurons from glutamate-induced neuronal toxicity. |
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| AbstractList | Glutamate excitotoxicity plays a crucial role in the pathogenesis behind the development and progression of several neurodegenerative diseases. The study aimed to investigate the neuroprotective activity of Gallic acid (GA) against glutamate-induced neurotoxicity in primary rat cortex neurons (RCN). Treated the RCNs with GA 25 & 50 μg/ml for 2 h and later treated the cells with 100 μM glutamate (GLU) and incubated for 24 h at 37 °C. The results demonstrated that, the GA improved the antioxidant profile in the cortex neurons and inhibited the production of the proinflammatory cytokine. GA also maintained the Ca
homeostasis, IGF-1 expression, and protected the neurons from glutamate-induced neuronal toxicity. The neuroprotective activity of GA has further confirmed from the results of N-acetylaspartate and expression of microtubule-associated protein-2 expression. The reports suggest that, GA is significantly attenuated the glutamate-induced neurotoxicity and protected neurons from various chemical events that are involved in the pathogenesis of neurotoxicity. Glutamate excitotoxicity plays a crucial role in the pathogenesis behind the development and progression of several neurodegenerative diseases. The study aimed to investigate the neuroprotective activity of Gallic acid (GA) against glutamate-induced neurotoxicity in primary rat cortex neurons (RCN). Treated the RCNs with GA 25 & 50 μg/ml for 2 h and later treated the cells with 100 μM glutamate (GLU) and incubated for 24 h at 37 °C. The results demonstrated that, the GA improved the antioxidant profile in the cortex neurons and inhibited the production of the proinflammatory cytokine. GA also maintained the Ca2+ homeostasis, IGF-1 expression, and protected the neurons from glutamate-induced neuronal toxicity. The neuroprotective activity of GA has further confirmed from the results of N-acetylaspartate and expression of microtubule-associated protein-2 expression. The reports suggest that, GA is significantly attenuated the glutamate-induced neurotoxicity and protected neurons from various chemical events that are involved in the pathogenesis of neurotoxicity.Glutamate excitotoxicity plays a crucial role in the pathogenesis behind the development and progression of several neurodegenerative diseases. The study aimed to investigate the neuroprotective activity of Gallic acid (GA) against glutamate-induced neurotoxicity in primary rat cortex neurons (RCN). Treated the RCNs with GA 25 & 50 μg/ml for 2 h and later treated the cells with 100 μM glutamate (GLU) and incubated for 24 h at 37 °C. The results demonstrated that, the GA improved the antioxidant profile in the cortex neurons and inhibited the production of the proinflammatory cytokine. GA also maintained the Ca2+ homeostasis, IGF-1 expression, and protected the neurons from glutamate-induced neuronal toxicity. The neuroprotective activity of GA has further confirmed from the results of N-acetylaspartate and expression of microtubule-associated protein-2 expression. The reports suggest that, GA is significantly attenuated the glutamate-induced neurotoxicity and protected neurons from various chemical events that are involved in the pathogenesis of neurotoxicity. Glutamate excitotoxicity plays a crucial role in the pathogenesis behind the development and progression of several neurodegenerative diseases. The study aimed to investigate the neuroprotective activity of Gallic acid (GA) against glutamate-induced neurotoxicity in primary rat cortex neurons (RCN). Treated the RCNs with GA 25 & 50 μg/ml for 2 h and later treated the cells with 100 μM glutamate (GLU) and incubated for 24 h at 37 °C. The results demonstrated that, the GA improved the antioxidant profile in the cortex neurons and inhibited the production of the proinflammatory cytokine. GA also maintained the Ca2+ homeostasis, IGF-1 expression, and protected the neurons from glutamate-induced neuronal toxicity. The neuroprotective activity of GA has further confirmed from the results of N-acetylaspartate and expression of microtubule-associated protein-2 expression. The reports suggest that, GA is significantly attenuated the glutamate-induced neurotoxicity and protected neurons from various chemical events that are involved in the pathogenesis of neurotoxicity. •Glutamate excitotoxicity is a major pathogenesis behind the development and progression of neurodegenerative diseases.•Glutamate-induced neurotoxicity in RCN is mediated through the formation of free radicles and proinflammatory cytokine.•Glutamate treatment also caused an alteration in Ca2+ homeostasis and decline in IGF-1 level.•Observed a down-regulation of MAP-2 expression and NAA concentration in glutamate treated rat cortex neurons.•Treatment with GA improved the antioxidant status in neurons and inhibited proinflammatory cytokine production.•GA also maintained the Ca2+ homeostasis, IGF-1 expression, and protected neurons from glutamate-induced neuronal toxicity. |
| Author | Maya, S. Prakash, T. Madhu, Krishnadas |
| Author_xml | – sequence: 1 givenname: S. surname: Maya fullname: Maya, S. – sequence: 2 givenname: T. surname: Prakash fullname: Prakash, T. email: prakasht@acharya.ac.in, mayas@acharya.ac.in – sequence: 3 givenname: Krishnadas orcidid: 0000-0002-1047-9153 surname: Madhu fullname: Madhu, Krishnadas |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30339985$$D View this record in MEDLINE/PubMed |
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| Keywords | sALS NO Neuronal protection HRP GLU Neurotoxicity MAP2 CSF NMDA GA GSH Glutamate excitotoxicity PBS Gallic acid Neurodegenerative diseases DTNB TMB IGF SOD EDTA NAA NOS ROS RCN GAPDH |
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| SubjectTerms | Gallic acid Glutamate excitotoxicity Neurodegenerative diseases Neuronal protection Neurotoxicity |
| Title | Assessment of neuroprotective effects of Gallic acid against glutamate-induced neurotoxicity in primary rat cortex neuronal culture |
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