Neuroprotective potential of carvacrol: restoration of oxidative balance and mitigation of brain injury markers in isoproterenol-induced rats

This research investigated the protective properties of Carvacrol (CVC) against Isoproterenol (ISO)-induced oxidative stress, neuroinflammation, and mitochondrial dysfunction in rats. The findings showed that CVC treatment did not significantly modify baseline oxidative stress levels in healthy rats but successfully alleviated ISO-induced oxidative damage by augmenting antioxidant enzyme activity and diminishing lipid peroxidation, as demonstrated by a reduction in MDA levels. These findings indicate that CVC can reinstate antioxidant capability and reduce oxidative damage. Concerning neuroinflammation, ISO therapy markedly increased the expression of pro-inflammatory markers, including TNF-alpha, IL-1 beta, c-Fos, BDNF, Nfl, and GFP, signifying a robust inflammatory and damage response. The injection of CVC following ISO exposure markedly decreased the expression of these markers, suggesting that CVC may exert a neuroprotective effect by regulating the inflammatory response and mitigating neuronal and glial damage. CVC demonstrated a notable protective effect on mitochondrial integrity, evidenced by the decreased mRNA expression of mitochondrial damage markers, including NSE, s100B, CALP1, and CALM1 in the CVC-treated groups, showing that CVC mitigates mitochondrial dysfunction. The analysis revealed no significant alterations in the expression levels of A beta 40, pTau181, and tTau across all groups, indicating that these biomarkers were not substantially influenced by CVC treatment under the study's conditions. However, beta-amyloid accumulation varied significantly between groups, highlighting the need for further research to explore CVC's potential implications in amyloid-related diseases. These findings endorse CVC's neuroprotective efficacy and therapeutic potential in neurological disorders associated with oxidative stress, inflammation, and mitochondrial impairment.

Journal

METABOLIC BRAIN DISEASE

Year

2025

Volume

40

Issue

5

ISSN

0885-7490

eISSN

1573-7365

DOI

10.1007/s11011-025-01634-6

WoS UID

WOS:001493464400002