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Objective <p>Breast cancer remains a significant global health challenge, despite advancements in chemotherapy. Targeted therapies utilizing plant-derived compounds are gaining attention, with Carvacrol—a monoterpene phenol—showing promise as an anticancer agent. This study evaluates Carvacrol antioxidant, anti-inflammatory, and pro-apoptotic effects in a DMBA-induced breast cancer rat model.</p> Method <p>Female rats were assigned to five groups: a normal/ healthy control (G1), a DMBA-induced cancer group monitored for 120 days (GII), and three tumor-bearing groups receiving Carvacrol (100&#xa0;mg/kg b.w.) via oral (GIII), intraperitoneal (GIV), or combined routes (GV), administered thrice weekly for 12 weeks.</p> Results <p>Carvacrol treatment markedly counteracted the detrimental effects induced by DMBA. Intraperitoneal administration produced the strongest therapeutic response, significantly enhancing apoptotic markers (cytochrome c, TNF-α, FADD) while suppressing anti-apoptotic proteins (Bcl-2, DR2). Pro-apoptotic regulators (p53, p73, TRAIL) were up regulated, confirming activation of the intrinsic apoptotic pathway. Carvacrol also attenuated lipid peroxidation by reducing malondialdehyde (MDA) levels, while boosting total antioxidant capacity and improving inflammatory status. Moreover, restoration of liver and kidney function was observed through normalization of serum ALT, AST, urea, and creatinine levels, together with improved histopathological architecture. Although the intraperitoneal route achieved the greatest efficacy, all routes of administration produced significant improvements compared with the untreated DMBA group, highlighting both the therapeutic potential of Carvacrol and the importance of bioavailability. Overall, Carvacrol suppresses DMBA-induced breast cancer through activation of intrinsic and extrinsic apoptotic pathways, reduction of oxidative stress, and protection of vital organs, with the injection route demonstrating the highest effectiveness.</p> Conclusion <p>The study supports Carvacrol potential as a complementary anticancer agent by enhancing apoptosis and reducing oxidative damage. Further research is required to optimize dosage and delivery for clinical applications.</p> Graphical abstract <p></p>

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Carvacrol-induced apoptosis via tumor suppressor gene activation and oxidative stress modulation in a rat model of breast cancer

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月10日

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  • Amany Elwakkad,
  • Amina A. Gamal el Din,
  • Mohamed A. Hebishy,
  • Howida S. Abou-Seif

摘要

Objective

Breast cancer remains a significant global health challenge, despite advancements in chemotherapy. Targeted therapies utilizing plant-derived compounds are gaining attention, with Carvacrol—a monoterpene phenol—showing promise as an anticancer agent. This study evaluates Carvacrol antioxidant, anti-inflammatory, and pro-apoptotic effects in a DMBA-induced breast cancer rat model.

Method

Female rats were assigned to five groups: a normal/ healthy control (G1), a DMBA-induced cancer group monitored for 120 days (GII), and three tumor-bearing groups receiving Carvacrol (100 mg/kg b.w.) via oral (GIII), intraperitoneal (GIV), or combined routes (GV), administered thrice weekly for 12 weeks.

Results

Carvacrol treatment markedly counteracted the detrimental effects induced by DMBA. Intraperitoneal administration produced the strongest therapeutic response, significantly enhancing apoptotic markers (cytochrome c, TNF-α, FADD) while suppressing anti-apoptotic proteins (Bcl-2, DR2). Pro-apoptotic regulators (p53, p73, TRAIL) were up regulated, confirming activation of the intrinsic apoptotic pathway. Carvacrol also attenuated lipid peroxidation by reducing malondialdehyde (MDA) levels, while boosting total antioxidant capacity and improving inflammatory status. Moreover, restoration of liver and kidney function was observed through normalization of serum ALT, AST, urea, and creatinine levels, together with improved histopathological architecture. Although the intraperitoneal route achieved the greatest efficacy, all routes of administration produced significant improvements compared with the untreated DMBA group, highlighting both the therapeutic potential of Carvacrol and the importance of bioavailability. Overall, Carvacrol suppresses DMBA-induced breast cancer through activation of intrinsic and extrinsic apoptotic pathways, reduction of oxidative stress, and protection of vital organs, with the injection route demonstrating the highest effectiveness.

Conclusion

The study supports Carvacrol potential as a complementary anticancer agent by enhancing apoptosis and reducing oxidative damage. Further research is required to optimize dosage and delivery for clinical applications.

Graphical abstract