Thymol attenuates carboplatin-induced nephrotoxicity in male rats by suppressing oxidative stress and NF-κB-mediated inflammation: A biochemical and histopathological study
- 1Department of Biology, College of Education for Pure Sciences, University of Anbar, Ramadi, Anbar, Iraq
Abstract
Objective: Carboplatin, a platinum-based chemotherapeutic agent, often causes dose‑limiting nephrotoxicity. Thymol, a natural monoterpene phenol, has antioxidant and anti‑inflammatory properties. This study aimed to determine whether thymol protects against carboplatin‑induced kidney injury in male rats.
Methods: Fifty adult male albino rats were randomly divided into five groups (n=10 each): control (distilled water), olive oil (vehicle), thymol alone (40 mg/kg/day orally), carboplatin alone (50 mg/kg single intraperitoneal), and carboplatin plus thymol (same doses, thymol started 24 hours after carboplatin). After three months, serum renal function markers, oxidative stress indices (malondialdehyde [MDA], 8‑hydroxy‑2′‑deoxyguanosine [8‑OHdG]), circulating Nrf2, antioxidant enzymes (superoxide dismutase [SOD], catalase [CAT], glutathione peroxidase [GPx], reduced glutathione [GSH]), pro‑inflammatory cytokines (NF‑κB p65, TNF‑α, IL‑6, IL‑1β), and renal histopathology were assessed. Data were analysed by one‑way ANOVA with Tukey’s post hoc test (p<0.05).
Results: Carboplatin significantly increased serum creatinine, urea, and uric acid; elevated MDA, 8‑OHdG, and circulating Nrf2; depleted SOD, CAT, GSH, and GPx; and raised NF‑κB, TNF‑α, IL‑6, and IL‑1β (p<0.05). Renal histology showed tubular degeneration, vascular congestion, and inflammatory infiltration. Co‑administration of thymol reversed most of these changes towards control values and markedly improved histological architecture.
Conclusion: Thymol attenuates carboplatin‑induced nephrotoxicity in male rats, likely by reducing oxidative damage and suppressing inflammatory signalling. These findings support further investigation of thymol as a potential adjunct to platinum‑based chemotherapy.
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BibTeX
@article{hameed2026thymol,
title = {{Thymol attenuates carboplatin-induced nephrotoxicity in male rats by suppressing oxidative stress and NF-κB-mediated inflammation: A biochemical and histopathological study}},
author = {Redhab Hameed and Haitham Abdulhadi},
journal = {Babcock University Medical Journal},
year = {2026},
month = oct,
doi = {10.38029/babcockuniv.med.j..v9is1.1652},
url = {https://doi.org/10.38029/babcockuniv.med.j..v9is1.1652},
note = {CC BY-NC},
}
RIS
TY - JOUR
TI - Thymol attenuates carboplatin-induced nephrotoxicity in male rats by suppressing oxidative stress and NF-κB-mediated inflammation: A biochemical and histopathological study
AU - Redhab Hameed
AU - Haitham Abdulhadi
PY - 2026
DA - 2026/10/01
JO - Babcock University Medical Journal
DO - 10.38029/babcockuniv.med.j..v9is1.1652
UR - https://doi.org/10.38029/babcockuniv.med.j..v9is1.1652
AB - Objective: Carboplatin, a platinum-based chemotherapeutic agent, often causes dose‑limiting nephrotoxicity. Thymol, a natural monoterpene phenol, has antioxidant and anti‑inflammatory properties. This study aimed to determine whether thymol protects against carboplatin‑induced kidney injury in male rats. Methods: Fifty adult male albino rats were randomly divided into five groups (n=10 each): control (distilled water), olive oil (vehicle), thymol alone (40 mg/kg/day orally), carboplatin alone (50 mg/kg single intraperitoneal), and carboplatin plus thymol (same doses, thymol started 24 hours after carboplatin). After three months, serum renal function markers, oxidative stress indices (malondialdehyde [MDA], 8‑hydroxy‑2′‑deoxyguanosine [8‑OHdG]), circulating Nrf2, antioxidant enzymes (superoxide dismutase [SOD], catalase [CAT], glutathione peroxidase [GPx], reduced glutathione [GSH]), pro‑inflammatory cytokines (NF‑κB p65, TNF‑α, IL‑6, IL‑1β), and renal histopathology were assessed. Data were analysed by one‑way ANOVA with Tukey’s post hoc test (p<0.05). Results: Carboplatin significantly increased serum creatinine, urea, and uric acid; elevated MDA, 8‑OHdG, and circulating Nrf2; depleted SOD, CAT, GSH, and GPx; and raised NF‑κB, TNF‑α, IL‑6, and IL‑1β (p<0.05). Renal histology showed tubular degeneration, vascular congestion, and inflammatory infiltration. Co‑administration of thymol reversed most of these changes towards control values and markedly improved histological architecture. Conclusion: Thymol attenuates carboplatin‑induced nephrotoxicity in male rats, likely by reducing oxidative damage and suppressing inflammatory signalling. These findings support further investigation of thymol as a potential adjunct to platinum‑based chemotherapy.
SN - 2465-6666
SN - 2756-4657
ER -