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April 3, 2026Food Science & Nutrition0 citationsOpen Access

Protective Effect of Silymarin Against Paclitaxel‐Induced Cardiotoxicity

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TTTuğçe TutarSYSeda YakutAKAdem Kara

Key Result

Silymarin mitigated Paclitaxel-induced cardiotoxicity in rats by reducing oxidative stress, inflammatory cytokines, and apoptosis markers while improving lipid profiles.

Key Points

  • The study investigates whether silymarin can protect against heart damage caused by paclitaxel treatment.
  • Rats were injected with paclitaxel to induce cardiotoxicity.
  • Silymarin was administered orally for 10 days following the paclitaxel treatment.
  • Biochemical assays measured levels of antioxidants and inflammatory cytokines.
  • Histopathological and immunohistochemical analyses were conducted on heart tissues.
  • Western blot analysis was used to assess protein expression related to inflammation and apoptosis.
  • Silymarin reduced malondialdehyde levels and increased antioxidant enzyme levels in heart tissue.
  • Decreased levels of inflammatory cytokines and improved lipid profiles were observed.
  • Histopathological analysis showed reduced inflammation in heart tissues.
  • Western blot results indicated downregulation of pro-inflammatory markers and an increase in the anti-apoptotic protein Bcl-2.

Structured PICO

Does silymarin mitigate paclitaxel-induced cardiotoxicity in a rat model?

P
Population
Rat model of Paclitaxel-induced cardiotoxicity (injected intraperitoneally with Paclitaxel at 2 mg/kg for five consecutive days)
I
Intervention
Silymarin administered orally at a dose of 200 mg/kg for 10 days (starting from day 6)
C
Comparator
Paclitaxel-treated rats without silymarin (implied by comparative results)
O
Outcome
Cardiotoxicity markers including oxidative stress (MDA, SOD, CAT, GPx, GSH), inflammation (cytokines, histopathology), lipid profiles, and apoptosis (Caspase-3, Bcl-2)surrogate

Silymarin demonstrates therapeutic potential in reducing paclitaxel-induced cardiotoxicity through antioxidant, anti-inflammatory, and anti-apoptotic mechanisms in a preclinical model.

Abstract

ABSTRACT Paclitaxel, a widely used chemotherapeutic agent, is known for its efficacy against various cancers but is also associated with significant cardiotoxicity. This study aimed to explore the potential of silymarin in mitigating Paclitaxel‐induced cardiotoxicity in rats. To establish a model of Paclitaxel‐induced cardiotoxicity, rats were injected intraperitoneally with Paclitaxel at 2 mg/kg for five consecutive days. Additionally, starting from day 6, silymarin was administered orally at a dose of 200 mg/kg for 10 days. Our findings indicate that silymarin reduced malondialdehyde (MDA) levels and increased the levels of antioxidant enzymes (SOD, CAT, GPx, and GSH) in heart tissue. Additionally, silymarin reduced serum cytokine levels (IL‐1β, TNF‐α, and IL‐6) and improved serum lipid profiles, reducing lactate dehydrogenase (LDH), high‐density lipoprotein (HDL), low‐density lipoprotein (LDL), triglyceride, and total cholesterol levels. Histopathological analysis revealed reduced inflammatory reaction scores in heart tissues. Immunohistochemical analysis revealed decreased PI3 kinase p85α scores, and western blot analysis showed downregulation of P2X7R, Interleukin‐1β (IL‐1β), Tumor Necrosis Factor‐α (TNF‐α), and nuclear factor kappa B p65 (NF‐κB‐p65) expression. Silymarin also reduced Caspase‐3 levels while increasing Bcl‐2 protein expression, an antiapoptotic protein. These results suggest that silymarin has significant therapeutic potential for reducing Paclitaxel‐induced cardiotoxicity via its antioxidant, anti‐inflammatory, and anti‐apoptotic properties.

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Cite This Study

Tutar et al. (2026) studied Paclitaxel-induced cardiotoxicity. Silymarin vs. Paclitaxel alone (implied) was evaluated on Cardiotoxicity markers (oxidative stress, cytokines, lipid profiles, histopathology, and apoptosis). Silymarin mitigated Paclitaxel-induced cardiotoxicity in rats by reducing oxidative stress, inflammatory cytokines, and apoptosis markers while improving lipid profiles.

synapsesocial.com/papers/69cf5e2e5a333a821460c50fhttps://doi.org/10.1002/fsn3.71710
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