Silymarin ameliorates post-weaning bisphenol A exposure-induced cardiotoxicity via suppression of TLR4/VCAM signaling in male Wistar rats.

This study assessed the cardiotoxic effect of post-weaning BPA exposure and the potential ameliorative effect of silymarin on BPA-induced cardiotoxicity. Twenty-four male Wistar rats were randomized into four groups: the control, silymarin-treated, bisphenol A (BPA)-treated, and the BPA+silymarin-treated. Post-weaning BPA exposure led to a rise in cardiac injury markers, malondialdehyde, and iron contents, and a reduction in GSH and GPX4. Moreover, BPA elevated cardiac TNF-α, IL-1β, MPO, VCAM-1, NF-kB, TLR4, caspase 3, cytochrome c, and DFI. Additionally, BPA promoted amyloid accumulation and distorted cardiac histoarchitecture. Nonetheless, silymarin treatment attenuated BPA-induced biochemical and histological alterations. In conclusion, silymarin attenuated BPA-induced cardiotoxicity, potentially via modulation of TLR4/VCAM signaling. Further studies are needed to confirm these mechanisms.