Palmatine attenuates LPS-induced inflammatory response in mouse mammary epithelial cells through inhibiting ERK1/2, P38 and Akt/NF-kB signalling pathways

Palmatine has a wide range of pharmacological effects and anti-inflammatory function. However, the effect of palmatine on LPS-induced inflammatory response of mammary epithelial cells has not been reported. In this research, we studied the anti-inflammatory mechanism of palmatine in EpH4-Ev (mouse mammary epithelial cells). EpH4-Ev cells were pre-treated with palmatine and then incubated with LPS. Cells were collected for examining production of pro-inflammatory mediators by qRT-PCR, and the related inflammatory signalling pathway was detected through immunofluorescence and Western blot. The results found that palmatine could significantly reduce the expression ofIL-6,TNF-alpha,IL-1 beta andCOX-2in EpH4-Ev cells. Research on mechanisms found that palmatine could significantly inhibit the protein levels of p-Akt, p-P65, p-ERK1/2 and p-P38 in EpH4-Ev cells. In conclusion, these data suggested that palmatine inhibits inflammatory response in LPS-induced EpH4-Ev cells via down-regulating Akt/ NF-kB, ERK1/2 and P38 signalling pathways.

Automated summary

The research showed that palmatine inhibits inflammatory response in LPS-induced mammary epithelial cells by down-regulating multiple inflammatory signaling pathways, including the expression of IL-6, TNF-alpha, IL-1 beta, and COX-2.