ArticleMetabolic brain disease2021
Carnosic acid depends on glutathione to promote mitochondrial protection in methylglyoxal-exposed SH-SY5Y cells.
Article in Metabolic brain disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- Dietary Carnosic Acid Supplementation Improves the Growth Performance, the Antioxidant Status, and Diversity of Intestinal Microbiota in Broilers.Antioxidants (Basel, Switzerland) · 2025Article
- Nrf2/Keap1/ARE regulation by plant secondary metabolites: a new horizon in brain tumor management.Cell communication and signaling : CCS · 2024Review
- Multi-Target Effects of ß-Caryophyllene and Carnosic Acid at the Crossroads of Mitochondrial Dysfunction and Neurodegeneration: From Oxidative Stress to Microglia-Mediated Neuroinflammation.Antioxidants (Basel, Switzerland) · 2022Review
- Modern aspects of the use of natural polyphenols in tumor prevention and therapy.Frontiers in cell and developmental biology · 2022Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Methylglyoxal (MG) is an endogenously produced toxicant that induces mitochondrial dysfunction leading to impaired redox biology homeostasis, bioenergetics collapse, and cell death in mammalian cells. However, MG toxicity is particularly relevant to neurons and glia given their chemical and metabolic characteristics. Here, we have investigated whether a pretreatment with carnosic acid (CA) would be able to promote mitochondrial protection in human neuroblastoma SH-SY5Y cells exposed to MG. We found that a pretreatment with CA at 1 μM for 12 h prevented the MG-induced lipid peroxidation and protein carbonylation and nitration in the membranes of mitochondria obtained from the SH-SY5Y cells. CA also prevented the MG-elicited Complexes I and V dysfunction, adenosine triphosphate (ATP) levels decline, and loss of mitochondrial membrane potential (MMP). Moreover, CA also reduced the mitochondrial production of the radical anion superoxide (O
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