Fumonisin B1 exposure induces apoptosis of human kidney tubular epithelial cells through regulating PTEN/PI3K/AKT signaling pathway via disrupting lipid raft formation.

Fumonisin B1 (FB1) is a fungal metabolite that causes a variety of toxicological effects to human and animals. In this study, we aimed to investigate the effects of FB1 on kidney injury and clarify the possible mechanism. Human kidney tubular epithelial cells (HK-2) were treated with FB1 for different concentrations. The results demonstrated that FB1 could suppress the viability of HK-2 cells. FB1 could lead to the apoptosis of HK-2 cells in a dose-dependent manner. Furthermore, treatment of FB1 could induce the production of ROS and MDA. And the levels of SOD and GSH were decreased by FB1. The expression of Caspase-3 and Bax increased markedly and BCL2 expression was decreased by FB1 treatment. In addition, FB1 treatment could up-regulate PTEN expression and down-regulate PI3K and AKT expression. Also, FB1 could disrupt lipid raft by decreasing sphingomyelin level. In conclusion, FB1 exposure induces apoptosis of HK-2 cells through regulating PTEN/PI3K/AKT signaling pathway via disrupting lipid raft formation.