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Peer-reviewedCC BY 4.0Journal of Biochemical and Molecular Toxicology

Nanocurcumin Attenuates Doxorubicin‐Induced Cardiotoxicity by Activating the Wnt/β‐Catenin/GSK‐3β Signaling Axis in Wistar Rats

  • Noha A. Alshuwayer1
  • Qamraa H. Alqahtani2
  • Marwa H. Hussein2
  • Raeesa Mohammed1
  • Abdulaziz Siyal1
  • Iman H. Hasan2
  1. 1Department of Anatomy, College of Medicine King Saud University Riyadh Saudi Arabia
  2. 2Department of Pharmacology and Toxicology, College of Pharmacy King Saud University Riyadh Saudi Arabia
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Abstract

Doxorubicin (DOX)–induced cardiotoxicity remains a major therapeutic limitation, emerging at the intersection of oxidative stress, mitochondrial impairment, and disruption of survival signaling pathways. The Wnt/β‑catenin–GSK‑3β pathway is an essential regulator of cardiomyocyte survival. To assess the cardioprotective potential of nanocurcumin (N‐Cur) in this condition, twenty‐four Wistar rats were divided into four groups (N‐Cur; 80 mg/kg, oral) was given for 2 weeks, while DOX was administered on day seven as a single dose. N‐Cur treatment significantly standardized DOX‑induced elevations in cTnI and CK‑MB, restored cardiac antioxidants (GSH, SOD), decreased MDA levels with p ≤ 0.01, significantly restored Nrf2, and reduced pro‑inflammatory mediators (TNF‑α, IL‑6, NF‑κB‑p65) (p < 0.001), thereby augmenting its twin roles as a potent anti‐inflammatory and antioxidant agent. The histopathological changes and inflammatory infiltration caused by DOX were significantly diminished following N‐Cur treatment. Further, DOX inhibited Wnt/β‑catenin signaling and increased GSK‑3β expression, whereas N‐Cur reversed these changes in immunohistochemistry studies. Collectively, these findings indicate that N‐Cur provides significant cardiomyocyte protection and efficiently modifies the Wnt/β‑catenin–GSK‑3β axis.

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Cite

BibTeXRIS
BibTeX
@article{alshuwayer2026nanocurcumin,
  title = {{Nanocurcumin Attenuates Doxorubicin‐Induced Cardiotoxicity by Activating the Wnt/β‐Catenin/GSK‐3β Signaling Axis in Wistar Rats}},
  author = {Noha A. Alshuwayer and Qamraa H. Alqahtani and Marwa H. Hussein and Raeesa Mohammed and Abdulaziz Siyal and Iman H. Hasan},
  journal = {Journal of Biochemical and Molecular Toxicology},
  year = {2026},
  month = nov,
  doi = {10.1002/jbt.71158},
  url = {https://doi.org/10.1002/jbt.71158},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Nanocurcumin Attenuates Doxorubicin‐Induced Cardiotoxicity by Activating the Wnt/β‐Catenin/GSK‐3β Signaling Axis in Wistar Rats
AU  - Noha A. Alshuwayer
AU  - Qamraa H. Alqahtani
AU  - Marwa H. Hussein
AU  - Raeesa Mohammed
AU  - Abdulaziz Siyal
AU  - Iman H. Hasan
PY  - 2026
DA  - 2026/11/04
JO  - Journal of Biochemical and Molecular Toxicology
DO  - 10.1002/jbt.71158
UR  - https://doi.org/10.1002/jbt.71158
AB  - Doxorubicin (DOX)–induced cardiotoxicity remains a major therapeutic limitation, emerging at the intersection of oxidative stress, mitochondrial impairment, and disruption of survival signaling pathways. The Wnt/β‑catenin–GSK‑3β pathway is an essential regulator of cardiomyocyte survival. To assess the cardioprotective potential of nanocurcumin (N‐Cur) in this condition, twenty‐four Wistar rats were divided into four groups (N‐Cur; 80 mg/kg, oral) was given for 2 weeks, while DOX was administered on day seven as a single dose. N‐Cur treatment significantly standardized DOX‑induced elevations in cTnI and CK‑MB, restored cardiac antioxidants (GSH, SOD), decreased MDA levels with p ≤ 0.01, significantly restored Nrf2, and reduced pro‑inflammatory mediators (TNF‑α, IL‑6, NF‑κB‑p65) (p < 0.001), thereby augmenting its twin roles as a potent anti‐inflammatory and antioxidant agent. The histopathological changes and inflammatory infiltration caused by DOX were significantly diminished following N‐Cur treatment. Further, DOX inhibited Wnt/β‑catenin signaling and increased GSK‑3β expression, whereas N‐Cur reversed these changes in immunohistochemistry studies. Collectively, these findings indicate that N‐Cur provides significant cardiomyocyte protection and efficiently modifies the Wnt/β‑catenin–GSK‑3β axis.
SN  - 1095-6670
SN  - 1099-0461
ER  -