Epimedium-derived icarisid I induces oxidative stress and nephrotoxicity by suppressing PI3K/AKT/Nrf2/HO-1 signaling pathway

Key Points

• Icarisid I exposure leads to significant oxidative stress in renal cells, contributing to nephrotoxicity.
• Specifically, the suppression of the PI3K/AKT/Nrf2/HO-1 signaling pathway was observed as a critical mechanism.
• Testing involved in vitro and in vivo components to evaluate the effects on renal function.
• Implications suggest potential renal damage risks related to icarisid I, requiring further investigation.