Eucommia ulmoides flavones (EUF) abrogated enterocyte damage induced by LPS involved in NF-κB signaling pathway.

This study was conducted to explore the regulatory mechanism of Eucommia ulmoides flavones (EUF) using enterocyte damage model induced by lipopolysaccharide (LPS). Intestinal porcine epithelial cell line (IPEC-J2) cells were cultured in Dulbecco's modified eagle medium with high glucose (DMEM-H) medium containing 0 or 10 μg/mL EUF, 0 or 40 ng/mL LPS. The results showed that LPS impaired DNA synthesis, cell viability, mitochondrial function, arrested cell cycle and induced apoptosis, reduced SOD activity while the EUF treated cells provided beneficial effect on all these parameters (P < 0.05). The addition of EUF increased phosphorylated Akt, IκBα and phosphorylated IKKα/β, but decreased Bax and Caspase-3 protein expressions in LPS-treated cells (P < 0.05). For the second experiment, cells were treated by DMEM-H medium containing 10 μg/mL EUF+ 40 ng/mL LPS or 10 μg/mL EUF+ 40 ng/mL LPS+ 10 μmol/L LY29400. EUF + LPS + LY29400 treatment significantly reduced cell viability, proliferation, mitochondrial bioenergetics parameters, SOD activity, and decreased protein expressions of PI3K, p-Akt, p-IKKα/β, p-NFκB and Bax (P < 0.05). These findings revealed the cytoprotective effects of EUF in enterocyte, which may involve the PI3K-NFκB signaling pathway, and it provides a theoretical basis for exploration of EUF as a potential anti-inflammatory compound to intervene intestinal inflammatory diseases.