Palmatine inhibits TRIF-dependent NF-κB pathway against inflammation induced by LPS in goat endometrial epithelial cells

- We identified that palmatine inhibits LPS-induced inflammatory reaction in goat endometrial epithelial cells (gEECs).
- The 10-227 μg/mL palmatine promotes the proliferation of gEECs.
- Palmatine suppress TRIF-dependent and TLR4 signaling pathways in gEECs.
- Palmatine can down-regulate the expression of NF-κB and suppress the action of NF-κBp65 in gEECs.
- In veterinary clinic, palmatine may be used to treat endometritis.

Palmatine, a natural pharmaceutical drug, possesses many biological activities. But its clinical application is rarely reported in the veterinary medicine. The aim of this study was to investigate the anti-inflammatory effects of palmatine on lipopolysaccharide (LPS)-induced inflammation in goat endometrial epithelial cells (gEECs), and the possible molecular mechanisms. Palmatine cell toxicity was determined by MTT assay, and the production of inflammatory cytokine in the cultured medium was measured with ELISA, qRT-PCR and Western blotting. Our results showed that palmatine treatment inhibited the release of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, nitric oxide (NO), matrix metalloproteinase (MMP)-9 and MMP-2. Furthermore, palmatine enhanced the secretion of prostaglandins E2 (PGE2) and IL-10. Palmatine significantly down-regulated the expression of Toll-like receptor 4 (TLR4), cluster of differentiation 14 (CD14), Toll/interleukin 1 receptor (TIR)-domain-containing adaptor protein inducing interferon-β (TICAM, TRIF) and nuclear factor-κB (NF-κB) in LPS stimulated gEECs, but did not alter the production of MyD88. In conclusion, palmatine inhibits TRIF-dependent NF-κB pathway to reduce LPS-induced inflammatory responses in goat endometrial epithelial cells.