Protective Effect of Silymarin Against Paclitaxel-Induced Cardiotoxicity.
Tuğçe Tutar1, Seda Yakut2, Adem Kara3
1Department of Physiology, Faculty of Veterinary Medicine Bingöl University Bingöl Türkiye.
Food Science & Nutrition
|April 6, 2026
Summary
Silymarin effectively mitigates Paclitaxel-induced cardiotoxicity in rats by reducing oxidative stress and inflammation. This natural compound demonstrates significant protective effects against chemotherapy-related heart damage.
Area of Science:
- Cardiovascular Pharmacology
- Natural Product Chemistry
- Oncology Supportive Care
Background:
- Paclitaxel is a vital chemotherapy drug with known cardiotoxicity.
- Developing strategies to counteract Paclitaxel-induced heart damage is crucial for cancer patient care.
Purpose of the Study:
- To investigate the cardioprotective potential of silymarin against Paclitaxel-induced cardiotoxicity in a rat model.
- To elucidate the underlying mechanisms of silymarin's protective effects.
Main Methods:
- Paclitaxel-induced cardiotoxicity model established in rats.
- Administration of silymarin and assessment of cardiac biomarkers, oxidative stress markers, inflammatory cytokines, lipid profiles, and histopathology.
- Immunohistochemical and Western blot analyses to evaluate key molecular pathways.
Main Results:
- Silymarin significantly reduced oxidative stress markers (MDA) and enhanced antioxidant enzyme activity (SOD, CAT, GPx, GSH).
- Silymarin decreased pro-inflammatory cytokines (IL-1β, TNF-α, IL-6) and improved lipid profiles (reduced LDH, LDL, triglycerides, total cholesterol).
- Silymarin treatment downregulated key inflammatory and apoptotic pathway proteins (P2X7R, IL-1β, TNF-α, NF-κB-p65, Caspase-3) and upregulated anti-apoptotic protein (Bcl-2).
Conclusions:
- Silymarin exhibits significant cardioprotective effects against Paclitaxel-induced cardiotoxicity.
- The protective mechanisms involve antioxidant, anti-inflammatory, and anti-apoptotic actions.
- Silymarin represents a promising therapeutic agent for managing chemotherapy-induced heart damage.


