ArticleJournal of neurotrauma2012
Carvacrol together with TRPC1 elimination improve functional recovery after traumatic brain injury in mice.
Article in Journal of neurotrauma, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- Carvacrol improves neurological function by inhibiting TRPM7-mediated BBB disruption and hemorrhage after TBI.Acta neuropathologica communications · 2025Article
- Gper1 inhibition exacerbates traumatic brain injury-induced neurological impairments in mice.Behavioral and brain functions : BBF · 2025Article
- Carvacrol Essential Oil as a Neuroprotective Agent: A Review of the Study Designs and Recent Advances.Molecules (Basel, Switzerland) · 2024Review
- The longitudinal biochemical profiling of TBI in a drop weight model of TBI.Scientific reports · 2023Article
- Therapeutics to Treat Psychiatric and Neurological Disorders: A Promising Perspective from Algerian Traditional Medicine.Plants (Basel, Switzerland) · 2023Review
- Satureja khuzistanica Jamzad essential oil and pure carvacrol attenuate TBI-induced inflammation and apoptosis via NF-κB and caspase-3 regulation in the male rat brain.Scientific reports · 2023Article
- Inhibition of transient receptor potential melastatin 7 (TRPM7) protects against Schwann cell trans-dedifferentiation and proliferation during Wallerian degeneration.Animal cells and systems · 2020Article
- The TRPC6 inhibitor, larixyl acetate, is effective in protecting against traumatic brain injury-induced systemic endothelial dysfunction.Journal of neuroinflammation · 2019Article
- TRPC1- and TRPC3-dependent CaGlia · 2017Article
- The anti-inflammatory properties of Satureja khuzistanica Jamzad essential oil attenuate the effects of traumatic brain injuries in rats.Scientific reports · 2016Article
- Role of TRP channels in the cardiovascular system.American journal of physiology. Heart and circulatory physiology · 2015Review
- Article
- A biocompatible "split luciferin" reaction and its application for non-invasive bioluminescent imaging of protease activity in living animals.Current protocols in chemical biology · 2014Article
- Traumatic brain injury using mouse models.Translational stroke research · 2014Review
- A biocompatible in vivo ligation reaction and its application for noninvasive bioluminescent imaging of protease activity in living mice.ACS chemical biology · 2013Article
- Neuroprotective effects of carvacrol against Alzheimer's disease and other neurodegenerative diseases: A review.Avicenna journal of phytomedicineReview
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Death of Central Nervous System (CNS) neurons following traumatic brain injury (TBI) is a complex process arising from a combination of factors, many of which are still unknown. It has been found that inhibition of transient receptor potential (TRP) channels constitutes an effective strategy for preventing death of CNS neurons following TBI. TRP channels are classified into seven related subfamilies, most of which are Ca(2+) permeable and involved in many cellular functions, including neuronal cell death. We hypothesized that TRP channels of the TRPC subfamily may be involved in post-TBI pathophysiology and that the compound 5-isopropyl-2-methylphenol (carvacrol), by inhibition of TRP channels, may exert neuroprotective effect after TBI. To test these suppositions, carvacrol was given to mice after TBI and its effect on their functional recovery was followed for several weeks. Our results show that neurological recovery after TBI was significantly enhanced by application of carvacrol. To better define the type of the specific channel involved, the effect of carvacrol on the extent and speed of recovery after TBI was compared among mice lacking TRPC1, TRPC3, or TRPC5, relative to wild type controls. We found that neurological recovery after TBI was significantly enhanced by combining carvacrol with TRPC1 elimination, but not by the absence of TRPC3 or TRPC5, showing a synergistic effect between carvacrol application and TRPC1 elimination. We conclude that TRPC1-sensitive mechanisms are involved in TBI pathology, and that inhibition of this channel by carvacrol enhances recovery and should be considered for further studies in animal models and humans.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.