Silibinin alleviates lipopolysaccharide induced inflammation in porcine mammary epithelial cells via mTOR/NF-κB signaling pathway.

SCOPE: Inflammatory responses reduce milk production in lactating sow. Silymarin (Silibinin is main component) reduced the inflammatory reaction and increased milk yield in lactating sow in our previous study. In the present study, we hypothesized that silibinin may be a previously unrecognized nutrients in inflammatory resolution in porcine mammary epithelial cells (PMECs).

METHODS AND RESULTS: PMECs were treated with or without lipopolysaccharide (LPS) in the absence or presence of silibinin to test cell viability, cell cycle, cell apoptosis, cellular inflammatory factors and signaling protein phosphorylation and expression. Silibinin promoted the proliferation of PMEC independent of the estrogen pathway. In LPS-induced damage of PMECs, silibinin protected cell proliferation, as well as reduced cell apoptosis. Silibinin reversed the LPS-induced increase in TNF-α expression compared with control. In addition, silibinin accentuated the LPS-induced decrease in the key proteins p-S6 and p-mTOR of the mTOR signaling pathway. Furthermore, silibinin reversed the increase in p-NF-κB p65, p-IκB-α and p-MAPK p38 expression in LPS-induced damage in PMECs.

CONCLUSION: This study highlights silibinin-mTOR/NF-κB axis plays an important role in the control of inflammation in PMECs, and suggests that silibinin may be an effective dietary strategy to alleviate the inflammatory response in lactating sow. This article is protected by copyright. All rights reserved.