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Silibinin Modulates NF-κB Activation and Heat Shock Protein in Preeclampsia-Like Rat Model
C F Bannwart-Castro1,2, M Romao-Veiga3,4, V R Ribeiro-Vasques3,4
1General and Applied Biology Post Graduate Program, Institute of Biosciences, Sao Paulo State University-UNESP, Botucatu, Sao Paulo, Brazil.
Insights
Silibinin, a natural flavonoid, shows promise in preventing preeclampsia (PE) by reducing inflammation and stress markers in a rat model. This study highlights silibinin
Area of Science:
- Reproductive biology and toxicology
- Pharmacology and natural product research
Background:
- Preeclampsia (PE) is a complex hypertensive disorder of pregnancy.
- PE pathophysiology involves placental oxidative stress and inflammation.
- Silibinin, a flavonoid, possesses antioxidant and anti-inflammatory properties.
Purpose of the Study:
- To investigate silibinin's preventive effects on N-nitro-L-arginine methyl ester (L-NAME)-induced preeclampsia in rats.
- To explore silibinin's potential as an anti-inflammatory agent for PE prevention.
Main Methods:
- Pregnant Wistar rats were induced with PE using L-NAME.
- Silibinin treatment was administered at different gestational stages (days 0, 7, or 14).
- Evaluated blood pressure, proteinuria, weight gain, and inflammatory markers (TNF-α, IL-1β, IFN-γ, Hsp70, NF-κB) in liver and placenta.
Main Results:
- Silibinin treatment significantly reduced levels of inflammatory cytokines (TNF-α, IL-1β, IFN-γ) and Hsp70 in liver and placenta.
- NF-κB activation was decreased in silibinin-treated groups, particularly when treatment started early.
- Silibinin demonstrated a preventive effect in this PE-like model.
Conclusions:
- Silibinin acts as a preventive agent in a PE-like rat model, mirroring key human PE features.
- The findings suggest silibinin modulates crucial inflammatory and stress pathways relevant to PE.
- Silibinin shows translational potential for preeclampsia prevention.
Problem:
Preeclampsia (PE) is a serious human pregnancy complication and remains the most complex hypertensive disorder due to its multifactorial nature and multisystemic effects. Despite the incomplete understanding of the PE pathophysiology, it is well-accepted that placental changes in PE are associated with oxidative stress, increasing the excessive production of cytokines and other inflammatory mediators. Thus, agents such as silibinin, a non-toxic natural polyphenolic flavonoid with antioxidant, anti-inflammatory, and hepatoprotective properties could modulate this profile for better disease resolution. This study aimed to investigate the effect of silibinin treatment on Nω-nitro-L-arginine methyl ester (L-NAME)-induced PE in rats, exploring its potential as a preventive anti-inflammatory agent.
Methods Of Study:
Pregnant Wistar rats were treated or not during gestation (days 10-19) with L-NAME (70-80 mg/kg/day) in drinking water and with silibinin (100 mg/kg/day, orally) starting on days 0, 7 or 14 of pregnancy. Systolic blood pressure was recorded on gestation days 0 and 20. The rats were euthanized on day 20. Then, we evaluated proteinuria, maternal weight gain, and litter weight. Tumor necrosis factor- alpha (TNF-α), interleukin-1 (IL-1β), IL-6, IL-10, interferon-gamma (IFN-γ), heat shock protein 70 (Hsp70) and NF-κB activity were determined in liver and placenta homogenates.
Results:
Our findings indicated that silibinin treatment decreased the production of the inflammatory cytokines TNF-α, IL-1β, IFN-γ, and reduced Hsp70 levels in the placenta and liver homogenate. NF-κB activation was also decreased in these organs of silibinin-treated groups, especially in the LN+SB0 and LN+SB7 groups.
Conclusion:
This study introduces a novel use of silibinin as a preventive agent in a PE-like model that reproduces essential features of human PE, providing physiological relevance to the findings. Overall, our data emphasize the translational potential of silibinin for PE prevention, showing promising effects on key inflammatory and stress-related pathways.
