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Peer-reviewedCC BYInternational journal of medical sciences

Effects of Resveratrol on Anxiety-Like Behavior, Neuronal Damage, and Apoptotic Signaling in Female Rats Exposed to Methylparaben.

  • Entesar AlShammari1
  • Promy Virk1
  • Dalal Alkhelb2
  • Fawaz Alasmari2
  • Wasayf Alotibi1
  • Nouf Alsultan3
  • Gadah Albasher1
  1. 1Department of Zoology, College of Science, King Saud University, Riyadh, Saudi Arabia.
  2. 2Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia.
  3. 3Faculty of Medicine and Health Sciences, Medical School, University of Nottingham, Nottingham NG7 2QL, UK.
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Abstract

Methylparaben (MEP), a widespread preservative, raises neurotoxicity concerns through oxidative stress and inflammation. Resveratrol (RES) is a natural polyphenol with antioxidant and anti-inflammatory properties. This study investigated whether RES protects against MEP-induced neurotoxicity in female rats. Female Wistar rats were divided into five groups (n=10/group): control, vehicle (5% DMSO), MEP alone (200 mg/kg, s.c., 15 days), RES alone (20 mg/kg, i.p., 15 days), and MEP+RES co-treatment. We evaluated anxiety-like behavior (elevated plus maze), brain histopathology (cortex/hippocampus), oxidative stress markers (GSH, SOD), stress-related gene expression (Nrf2, ASK1, PP-1cs, PP-2Acs by qPCR), inflammatory proteins (TNF-α, IL-6 by immunohistochemistry), and apoptotic markers (BAX, BCL-2). MEP exposure significantly increased anxiety-like behavior, caused structural damage in cortex and hippocampus, depleted GSH and SOD, upregulated Nrf2, ASK1, PP-1cs, and PP-2Acs, elevated TNF-α, IL-6, and pro-apoptotic BAX, while reducing BCL-2. RES alone caused no adverse effects. Remarkably, RES co-administration significantly attenuated and partially restored MEP-induced alterations, restoring behavior, tissue architecture, antioxidant defenses, gene expression, and immune balance. RES effectively attenuates MEP-induced neurotoxicity through antioxidant, anti-inflammatory, and anti-apoptotic mechanisms, positioning it as a promising neuroprotective agent against environmental toxicants.

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Cite

BibTeXRIS
BibTeX
@article{alshammari2026effects,
  title = {{Effects of Resveratrol on Anxiety-Like Behavior, Neuronal Damage, and Apoptotic Signaling in Female Rats Exposed to Methylparaben.}},
  author = {Entesar AlShammari and Promy Virk and Dalal Alkhelb and Fawaz Alasmari and Wasayf Alotibi and Nouf Alsultan and Gadah Albasher},
  journal = {International journal of medical sciences},
  year = {2026},
  month = sep,
  doi = {10.7150/ijms.138134},
  url = {https://europepmc.org/article/MED/42909400},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Effects of Resveratrol on Anxiety-Like Behavior, Neuronal Damage, and Apoptotic Signaling in Female Rats Exposed to Methylparaben.
AU  - Entesar AlShammari
AU  - Promy Virk
AU  - Dalal Alkhelb
AU  - Fawaz Alasmari
AU  - Wasayf Alotibi
AU  - Nouf Alsultan
AU  - Gadah Albasher
PY  - 2026
DA  - 2026/09/03
JO  - International journal of medical sciences
DO  - 10.7150/ijms.138134
UR  - https://europepmc.org/article/MED/42909400
AB  - Methylparaben (MEP), a widespread preservative, raises neurotoxicity concerns through oxidative stress and inflammation. Resveratrol (RES) is a natural polyphenol with antioxidant and anti-inflammatory properties. This study investigated whether RES protects against MEP-induced neurotoxicity in female rats. Female Wistar rats were divided into five groups (n=10/group): control, vehicle (5% DMSO), MEP alone (200 mg/kg, s.c., 15 days), RES alone (20 mg/kg, i.p., 15 days), and MEP+RES co-treatment. We evaluated anxiety-like behavior (elevated plus maze), brain histopathology (cortex/hippocampus), oxidative stress markers (GSH, SOD), stress-related gene expression (Nrf2, ASK1, PP-1cs, PP-2Acs by qPCR), inflammatory proteins (TNF-α, IL-6 by immunohistochemistry), and apoptotic markers (BAX, BCL-2). MEP exposure significantly increased anxiety-like behavior, caused structural damage in cortex and hippocampus, depleted GSH and SOD, upregulated Nrf2, ASK1, PP-1cs, and PP-2Acs, elevated TNF-α, IL-6, and pro-apoptotic BAX, while reducing BCL-2. RES alone caused no adverse effects. Remarkably, RES co-administration significantly attenuated and partially restored MEP-induced alterations, restoring behavior, tissue architecture, antioxidant defenses, gene expression, and immune balance. RES effectively attenuates MEP-induced neurotoxicity through antioxidant, anti-inflammatory, and anti-apoptotic mechanisms, positioning it as a promising neuroprotective agent against environmental toxicants.
SN  - 1449-1907
ER  -