ArticleNeurotoxicity research2023
The Effects of Carvacrol on Transient Receptor Potential (TRP) Channels in an Animal Model of Parkinson's Disease.
Article in Neurotoxicity research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Intranasal 6-OHDA Induces TRPM3-mediated Neuroinflammation in the pVTA: A Preclinical Early-stage Parkinson's Disease Model.Molecular neurobiology · 2026Article
- TFAM signaling molecule alleviates mitochondrial damage of cerebral ischemia-reperfusion.Cell death discovery · 2026Article
- Plant-Derived Monoterpene Therapies in Parkinson's Disease Models: Systematic Review and Meta-Analysis.Plants (Basel, Switzerland) · 2025Review
- Carvacrol improves cognitive dysfunction by decreasing amyloid-β accumulation and regulating neuroinflammation in ovariectomized renovascular hypertensive rats.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Carvacrol Essential Oil as a Neuroprotective Agent: A Review of the Study Designs and Recent Advances.Molecules (Basel, Switzerland) · 2024Review
- Modulation of TRPV1 and TRPA1 Channels Function by Sea Anemones' Peptides Enhances the Viability of SH-SY5Y Cell Model of Parkinson's Disease.International journal of molecular sciences · 2023Article
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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
In this study, we aimed to investigate the effects of carvacrol (CA), a widely used phytochemical having anti-oxidant and neuroprotective effects, on transient receptor potential (TRP) channels in an animal model of Parkinson's disease (PD). A total of 64 adult male Spraque-Dawley rats were divided into four groups: sham-operated, PD animal model (unilateral intrastriatal injections of 6-hydroxydopamine (6-OHDA), 6 µg/µl), PD + vehicle (dimethyl sulfoxide (DMSO)) treatment, and PD + CA treatment (10 mg/kg, every other day, for 14 days). Half of the brain samples of substantia nigra pars compacta (SNpc) and striatum (CPu) were collected for immunohistochemistry and the remaining half were used for molecular analyses. CA treatment significantly increased the density of dopaminergic neurons immunolabeled with tyrosine hydroxylase and transient receptor potential canonical 1 (TRPC1) channel in the SNpc of PD animals. In contrast, the density of astrocytes immunolabeled with glial fibrillary acetic acid and transient receptor potential ankyrin 1 (TRPA1) channel significantly decreased following CA treatment in the CPu of PD animals. RT-PCR and western blot analyses showed that 6-OHDA administration significantly reduced TRPA1 and TPRPC1 mRNA expression and protein levels in both SNpc and CPu. CA treatment significantly upregulated TRPA1 expression in PD group, while TRPC1 levels did not display an alteration. Based on this data it was concluded that CA treatment might protect the number of dopaminergic neurons by reducing the reactive astrogliosis and modulating the expression of TRP channels in both neurons and astrocytes in an animal model of PD.
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