# Role of Thymus ciliatus (Thyme) to Ameliorate the Acute Neurotoxicity Induced by Bisphenol A: In Vivo Supported with Virtual Study

**Authors:** Dallal Kourat, Djallal Eddine H. Adli, Mostapha Brahmi, Faisal K. Alkholifi, Faten F. Bin Dayel, Wafaa Arabi, Marie-Laure Fauconnier, Bakhta Bouzouira, Khaled Kahloula, Miloud Slimani, Sherouk Hussein Sweilam

PMC · DOI: 10.3390/ph18040509 · Pharmaceuticals · 2025-03-31

## TL;DR

This study shows that Thymus ciliatus essential oil can reduce the harmful effects of bisphenol A on the brain and behavior in rats, suggesting potential therapeutic uses.

## Contribution

The study introduces Thymus ciliatus essential oil as a potential therapeutic agent against BPA-induced neurotoxicity.

## Key findings

- BPA exposure caused neurobehavioral impairments, stress, anxiety, and memory deficits in rats.
- Thymus ciliatus essential oil treatment reversed BPA-induced behavioral and metabolic disturbances.
- Molecular docking suggests TEO interacts with key enzymes and receptors, offering a possible mechanism for its protective effects.

## Abstract

Background/Objectives: The purpose of this research was to investigate the effects of bisphenol A (BPA) exposure on neurobehavioral testing in young Wistar rats and to evaluate the therapeutic potential of Thymus ciliatus (TEO) essential oil to attenuate the damage induced by this chemical toxin. Methods: The essential oil was extracted by hydro-distillation (yield of 2.26%), and the characterization by GC-MS indicates that the major components of Thymus ciliatus oil are thymol (63.33%), p-cymene (13.4%), and σ-terpinene (6.69%). Acute BPA intoxication was induced with a dose of 50 mg/kg orally for 60 days. The neurobehavioral evaluation, performed using a comprehensive set of tests including the forced swim test, dark/light box, Morris water maze, open field test, and sucrose preference test, clearly demonstrated that bisphenol A (BPA) exposure induced significant neurobehavioral impairments. Results: These impairments included reduced exploratory behavior indicative of heightened stress, anxiety, and depressive-like states, as well as deficits in memory and learning. Furthermore, BPA intoxication was associated with metabolic disturbances such as hyperglycemia along with histopathological evidence of brain tissue damage. However, TEO treatment attenuated these adverse effects by restoring neurobehavioral function. Molecular docking analysis revealed an affinity between the major essential oils identified in T. ciliatus, BPA, and the 5HT2C receptor and the MAO, AChE, and BChE enzymes, suggesting a potential mechanism underlying BPA’s effects on behavior and memory. In addition, TEO also showed an interaction with these molecules, suggesting a therapeutic potential against BPA. These findings underscore the promising role of TEO in mitigating the poisonous effects of BPA and pave the way for additional research into the molecular mechanisms and therapeutic uses of natural bioactive compounds for the prevention and treatment of toxic diseases. Thymol, the major compound in TEO, exhibited activity related to the dopamine and serotonin pathways, so it could have potential antidepressant properties. Conclusions: Thymol might be a promising candidate for the treatment of neurodegenerative and neurological disorders such as depression, Parkinson’s disease, and Alzheimer’s disease while also preventing histological damage in the brain.

## Linked entities

- **Chemicals:** bisphenol A (PubChem CID 6623), thymol (PubChem CID 6989), p-cymene (PubChem CID 7463)
- **Diseases:** depression (MONDO:0002050), Parkinson’s disease (MONDO:0005180), Alzheimer’s disease (MONDO:0004975)

## Full-text entities

- **Genes:** Maoa (monoamine oxidase A) [NCBI Gene 29253] {aka Mao}, Ache (acetylcholinesterase) [NCBI Gene 83817], Bche (butyrylcholinesterase) [NCBI Gene 65036]
- **Diseases:** neurodegenerative and neurological disorders (MESH:D020271), hyperglycemia (MESH:D006943), anxiety (MESH:D001007), depression (MESH:D003866), Alzheimer's disease (MESH:D000544), toxic diseases (MESH:D004194), neurobehavioral impairments (MESH:D019954), Neurotoxicity (MESH:D020258), Parkinson's disease (MESH:D010300), deficits in memory and learning (MESH:D007859)
- **Species:** Rattus norvegicus (brown rat, species) [taxon 10116]

## Full text

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## Figures

11 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12030012/full.md

## References

80 references — full list in the complete paper: https://tomesphere.com/paper/PMC12030012/full.md

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Source: https://tomesphere.com/paper/PMC12030012