ArticleExperimental neurology2015
Nrf2-ARE activator carnosic acid decreases mitochondrial dysfunction, oxidative damage and neuronal cytoskeletal degradation following traumatic brain injury in mice.
Article in Experimental neurology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
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Who cites it
48 citing papers in PubMed, 95 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
- Carnosol, a Rosemary Ingredient Discovered in a Screen for Inhibitors of SARM1-NADAntioxidants (Basel, Switzerland) · 2025Article
- The Cerebral Protective Effect of Novel Erinacines fromAntioxidants (Basel, Switzerland) · 2024Article
- Neuroprotection of NRF2 against Ferroptosis after Traumatic Brain Injury in Mice.Antioxidants (Basel, Switzerland) · 2023Article
- Neuroprotective Effects of Carnosic Acid: Insight into Its Mechanisms of Action.Molecules (Basel, Switzerland) · 2023Review
- Anti-Inflammatory Therapeutic Mechanisms of Natural Products: Insight from Rosemary Diterpenes, Carnosic Acid and Carnosol.Biomedicines · 2023Review
- Beta1-receptor blockade attenuates atherosclerosis progression following traumatic brain injury in apolipoprotein E deficient mice.PloS one · 2023Article
- 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
- Targeting Nrf2-Mediated Oxidative Stress Response in Traumatic Brain Injury: Therapeutic Perspectives of Phytochemicals.Oxidative medicine and cellular longevity · 2022Review
- Mitochondrial dysfunction in perinatal asphyxia: role in pathogenesis and potential therapeutic interventions.Molecular and cellular biochemistry · 2021Review
- Huperzine A protects against traumatic brain injury through anti-oxidative effects via the Nrf2-ARE pathway.Iranian journal of basic medical sciences · 2021Article
- Article
- Polydatin Attenuates OGD/R-Induced Neuronal Injury and Spinal Cord Ischemia/Reperfusion Injury by Protecting Mitochondrial Function via Nrf2/ARE Signaling Pathway.Oxidative medicine and cellular longevity · 2021Article
- Astaxanthin provides neuroprotection in an experimental model of traumatic brain injury via the Nrf2/HO-1 pathway.American journal of translational research · 2021Article
- Article
- Revisiting Traumatic Brain Injury: From Molecular Mechanisms to Therapeutic Interventions.Biomedicines · 2020Review
- Repetitive Mild Traumatic Brain Injury and Transcription Factor Modulation.Journal of neurotrauma · 2020Article
- Idebenone Has Distinct Effects on Mitochondrial Respiration in Cortical Astrocytes Compared to Cortical Neurons Due to Differential NQO1 Activity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Transcriptional activation of antioxidant gene expression by Nrf2 protects against mitochondrial dysfunction and neuronal death associated with acute and chronic neurodegeneration.Experimental neurology · 2020Review
- An Effective NADPH Oxidase 2 Inhibitor Provides Neuroprotection and Improves Functional Outcomes in Animal Model of Traumatic Brain Injury.Neurochemical research · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The importance of free radical-induced oxidative damage after traumatic brain injury (TBI) has been well documented. Despite multiple clinical trials with radical-scavenging antioxidants that are neuroprotective in TBI models, none is approved for acute TBI patients. As an alternative antioxidant target, Nrf2 is a transcription factor that activates expression of antioxidant and cytoprotective genes by binding to antioxidant response elements (AREs) within DNA. Previous research has shown that neuronal mitochondria are susceptible to oxidative damage post-TBI, and thus the current study investigates whether Nrf2-ARE activation protects mitochondrial function when activated post-TBI. It was hypothesized that administration of carnosic acid (CA) would reduce oxidative damage biomarkers in the brain tissue and also preserve cortical mitochondrial respiratory function post-TBI. A mouse controlled cortical impact (CCI) model was employed with a 1.0mm cortical deformation injury. Administration of CA at 15 min post-TBI reduced cortical lipid peroxidation, protein nitration, and cytoskeletal breakdown markers in a dose-dependent manner at 48 h post-injury. Moreover, CA preserved mitochondrial respiratory function compared to vehicle animals. This was accompanied by decreased oxidative damage to mitochondrial proteins, suggesting the mechanistic connection of the two effects. Lastly, delaying the initial administration of CA up to 8h post-TBI was still capable of reducing cytoskeletal breakdown, thereby demonstrating a clinically relevant therapeutic window for this approach. This study demonstrates that pharmacological Nrf2-ARE induction is capable of neuroprotective efficacy when administered after TBI.
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