ArticleNeurotoxicity research2019
Carnosic Acid Pretreatment Attenuates Mitochondrial Dysfunction in SH-SY5Y Cells in an Experimental Model of Glutamate-Induced Excitotoxicity.
Article in Neurotoxicity research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Acai Berry Extracts Can Mitigate the L-Glutamate-Induced Neurotoxicity Mediated by N-Methyl-D-Aspartate Receptors.Brain sciences · 2025Article
- Neuroprotective Riluzole-Releasing Electrospun Implants for Spinal Cord Injury.Molecular pharmaceutics · 2025Article
- Nrf2/Keap1/ARE regulation by plant secondary metabolites: a new horizon in brain tumor management.Cell communication and signaling : CCS · 2024Review
- Carnosic Acid Shows Higher Neuroprotective Efficiency than Edaravone or Ebselen in In Vitro Models of Neuronal Cell Damage.Molecules (Basel, Switzerland) · 2023Article
- Acai Berry (Life (Basel, Switzerland) · 2023Article
- Neuroprotective Effects of Carnosic Acid: Insight into Its Mechanisms of Action.Molecules (Basel, Switzerland) · 2023Review
- Is L-Glutamate Toxic to Neurons and Thereby Contributes to Neuronal Loss and Neurodegeneration? A Systematic Review.Brain sciences · 2022Review
- Modern aspects of the use of natural polyphenols in tumor prevention and therapy.Frontiers in cell and developmental biology · 2022Review
- Potential of Medicinal Plants as Neuroprotective and Therapeutic Properties Against Amyloid-β-Related Toxicity, and Glutamate-Induced Excitotoxicity in Human Neural Cells.Current neuropharmacology · 2021Review
- Mitochondrial Protection Promoted by the Coffee Diterpene Kahweol in Methylglyoxal-Treated Human Neuroblastoma SH-SY5Y Cells.Neurotoxicity research · 2020Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondria are the major site of adenosine triphosphate (ATP) production in mammalian cells. Moreover, mitochondria produce most of the reactive oxygen species (ROS) in nucleated cells. Redox and bioenergetic abnormalities have been seen in mitochondria during the onset and progression of neurodegenerative diseases. In that context, excitotoxicity induced by glutamate (GLU) plays an important role in mediating neurotoxicity. Several drugs have been used in the treatment of diseases involving excitotoxicity. Nonetheless, some patients (20-30%) present drug resistance. Thus, it is necessary to find chemicals able to attenuate mitochondrial dysfunction in the case of excitotoxicity. In this work, we treated the human neuroblastoma SH-SY5Y cell line with the diterpene carnosic acid (CA) at 1 μM for 12 h prior to the exposure to GLU for further 24 h. We found that CA prevented the GLU-induced mitochondrion-related redox impairment and bioenergetic decline in SH-SY5Y cells. CA also downregulated the pro-apoptotic stimulus elicited by GLU in this experimental model. CA exerted mitochondrial protection by a mechanism associated with the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2), since silencing of this protein with small interfering RNA (siRNA) suppressed the CA-induced protective effects. Future directions include investigating whether CA would be able to modulate mitochondrial function and/or dynamics in in vivo experimental models of excitotoxicity.
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